PAIN-TYPES, PATHWAY,
THEORIES & MODULATION
DR. MUMUX MIRANI
BPT, MPT SPORTS, PHD SCHOLAR,
ASSISTANT PROFESSOR,
SPB PHYSIOTHERAPY COLLEGE, SURAT.
PAIN MEANS?
•Gujarati – દુઃખ
•Sanskrit - पीडा
•Hindi - वेदना
•Urdu – दर्द
•Spanish – dolor
•Russian – боль (bol)
PAIN
MEANS???
PAIN
MEANS???
BASIC DEFINITION
•Pain is an unpleasant sensory and emotional
experience associated with actual or potential
tissue damage.
TYPES OF PAIN
*Le you in pain
*Chronic pain
*Acute pain
* Nociceptive pain
*Visceral pain
*Neuropathic pain
TYPES OF PAIN:
• 1. Acute Pain: Short-term, resolves with healing (e.g., injury,
surgery)
• 2. Chronic Pain: Long-term, persists beyond healing (e.g., arthritis,
fibromyalgia)
• 3. Nociceptive Pain: Caused by tissue damage (e.g., burns, cuts)
• 4. Neuropathic Pain: Resulting from nerve damage (e.g., diabetes,
shingles)
• 5. Visceral Pain: Originating from internal organs (e.g.,
appendicitis, kidney stones)
1. ACUTE PAIN
•- Duration: Short-term, usually less than 3-6 months
•- Cause: Injury, surgery, infection, or inflammation
•- Characteristics: - Sudden onset
•- Sharp, stabbing, or aching sensation
•- Usually resolves with healing
•- Example: post-operative pain, broken bone, or acute
appendicitis
2. CHRONIC PAIN
•- Duration: Long-term, persists beyond 3-6 months
•- Cause: Ongoing conditions like arthritis, fibromyalgia, or
nerve damage
Characteristics:
•- Persistent or recurring pain
•- Can be dull, aching, or burning
•- Impacts daily life and mental health
•Example: chronic back pain, arthritis, or fibromyalgia
3. NOCICEPTIVE PAIN
- Cause: Tissue damage or inflammation
Characteristics:
- Sharp, stabbing, or aching sensation
- Usually localized to the affected area
-Example: burns, cuts, fractures, or sprains-
Subtypes:
-Somatic nociceptive pain (skin, muscles, bones)
-Visceral nociceptive pain (internal organs)
4. NEUROPATHIC PAIN-
•Cause: Nerve damage or dysfunction
Characteristics:
•- Burning, shooting, or stabbing sensation
•- Can be spontaneous or triggered by stimuli
•- Often accompanied by numbness, tingling, or weakness
•- Example: diabetic neuropathy, shingles, or multiple
sclerosis
5. VISCERAL PAIN
•- Origin: Internal organs (e.g., abdomen, thorax, pelvis)
•- Cause: Inflammation, infection, or obstruction
•- Characteristics:
•- Dull, aching, or cramping sensation
•- Often referred to other areas (e.g., shoulder pain from
gallbladder issue)
•- Example: appendicitis, kidney stones, or inflammatory
bowel disease
PAIN PATHWAYS???
PAIN PATHWAY FLOWCHART
1. TRANSDUCTION-
• Nociceptors: Specialized nerve endings that detect tissue damage,
inflammation, or other harmful stimuli
• Activation: Nociceptors respond to various stimuli, such as:
- Mechanical (pressure, stretch, vibration)
- Thermal (heat, cold)
- Chemical (inflammation, toxins)
- Electrical (direct stimulation)
- Signalling: Activated nociceptors release neurotransmitters, like substance P
and calcitonin gene-related peptide (CGRP), which transmit signals to the
spinal cord
2. TRANSMISSION
• - Spinal Cord: Signals from nociceptors enter the spinal cord through dorsal
roots
• Ascending Pathways: Signals ascend through the spinal cord via:
- Spinothalamic tract (STT): transmits pain, temperature, and touch information
- Spinoreticular tract (SRT): involved in pain modulation and emotional response
- Spinomesencephalic tract (SMT): transmits pain information to the brainstem
- Nerve Fibers: Signals travel through A-delta (A )
δ and C fibers:
- Aδ fibers: fast, myelinated fibers transmitting sharp, localized pain
- C fibers: slow, unmyelinated fibers transmitting dull, aching pain
3. PERCEPTION
• - Brainstem: Signals reach the brainstem, where they're processed and modified by
various structures:
• Periaqueductal gray (PAG): involved in pain modulation and emotional response
• Reticular formation: regulates arousal, attention, and pain perception
- Thalamus: Signals relayed to the thalamus, which acts as a sensory processing hub
- Cortex: Signals reach the somatosensory cortex, where pain is perceived and
interpreted:
- Primary somatosensory cortex (SI): processes basic sensory information
- Secondary somatosensory cortex (SII): involved in pain localization and intensity
- Insula: contributes to pain emotion, empathy, and interoception
• The brain interprets these signals as pain, taking into account various
factors, such as:
- Intensity
- Duration
- Location
- Quality (sharp, dull, burning, etc.)
- Emotional state
- Past experiences
- Expectations
- This complex process allows us to perceive and respond to pain, enabling
us to protect ourselves from harm and maintain homeostasis.
3 THEORIES OF PAIN:
1. Specificity Theory
2. Pattern Theory
3. Gate Control Theory
1. SPECIFICITY THEORY
• Proposed by: Max von Frey (1894)
• Key idea: Pain is a specific sensation with its own dedicated receptors and pathways
• Assumptions:
- Pain has its own unique sensory system
- Nociceptors detect specific painful stimuli
- Signals transmitted through specific pain pathways-
• Strengths:
- Explains why pain is a distinct sensation
- Supports the existence of nociceptors
• Weaknesses:
- Oversimplifies pain processing
- Doesn't account for individual differences in pain perception
2. PATTERN THEORY
• Proposed by: Ronald Melzack and Patrick Wall (1962)
• -Key idea: Pain is a pattern of nerve activity interpreted by the brain
• Assumptions:
- Pain is a complex sensory experience
- Nerve activity patterns are decoded by the brain
- Context and past experiences influence pain perception
- Strengths: - Recognizes pain's subjective nature - Emphasizes the role
of brain processing
- Weaknesses: - Difficult to test and quantify - Doesn't fully explain
pain mechanisms
3. GATE CONTROL THEORY
• Proposed by: Ronald Melzack and Patrick Wall (1965)
• Key idea: Pain is modulated by the brain's ability to gate or block signals-
• Assumptions:
- Pain signals can be blocked or reduced by other sensory inputs
- The brain acts as a "gate" controlling pain transmission
- Activation of certain nerves can close the gate, reducing pain
• Strengths:
- Explains pain modulation and relief
- Supports the use of alternative therapies (e.g., acupuncture)
• Weaknesses:
- Oversimplifies pain mechanisms
- Doesn't fully account for individual differences
PAIN MODULATION:
1. Ascending Pain Modulation
2. Descending Pain Modulation
3. Segmental Pain Modulation
1. ASCENDING PAIN MODULATION
• Signals from nociceptors transmit to the spinal cord and brain
• Ascending pathways:
- Spinothalamic tract (STT): transmits pain, temperature, and touch
- Spinoreticular tract (SRT): involved in pain modulation and emotional
response
- Spinomesencephalic tract (SMT): transmits pain information to the brainstem
• Brain regions involved:
- Thalamus: relays sensory information
- Somatosensory cortex: processes pain location and intensity
- Limbic system: processes emotional aspects of pain
2. DESCENDING PAIN MODULATION
• Brain sends signals to reduce pain transmission
• Mechanisms:
- Endogenous opioids (endorphins, enkephalins): natural painkillers
- Opioid receptors: activated by opioids, reducing pain transmission
- Monoamine systems (serotonin, noradrenaline): regulate pain modulation
• Descending pathways:
- Periaqueductal gray (PAG): sends signals to spinal cord to reduce pain
- Reticular formation: regulates arousal and pain modulation
- Rostral ventromedial medulla (RVM): sends signals to spinal cord to reduce
pain
3. SEGMENTAL PAIN MODULATION
•Local spinal cord mechanisms modulate pain
•Mechanisms:
- Inhibition: reducing pain transmission
- Facilitation: enhancing pain transmission
- Gating: controlling pain transmission-
•Segmental pathways:
- Dorsal horn: receives and processes pain information
- Ventral horn: sends signals to muscles and glands
- Spinal interneurons: regulate pain modulation
SIDE NOTES:
•These pain modulation mechanisms interact and coordinate
to regulate pain perception.
•Understanding these processes helps develop effective
pain management strategies, including pharmacological
and non-pharmacological interventions.
THANK YOU.

Pain-Types, pathway, theories & modulation.pptx

  • 1.
    PAIN-TYPES, PATHWAY, THEORIES &MODULATION DR. MUMUX MIRANI BPT, MPT SPORTS, PHD SCHOLAR, ASSISTANT PROFESSOR, SPB PHYSIOTHERAPY COLLEGE, SURAT.
  • 2.
    PAIN MEANS? •Gujarati –દુઃખ •Sanskrit - पीडा •Hindi - वेदना •Urdu – दर्द •Spanish – dolor •Russian – боль (bol)
  • 3.
  • 4.
  • 5.
    BASIC DEFINITION •Pain isan unpleasant sensory and emotional experience associated with actual or potential tissue damage.
  • 6.
    TYPES OF PAIN *Leyou in pain *Chronic pain *Acute pain * Nociceptive pain *Visceral pain *Neuropathic pain
  • 7.
    TYPES OF PAIN: •1. Acute Pain: Short-term, resolves with healing (e.g., injury, surgery) • 2. Chronic Pain: Long-term, persists beyond healing (e.g., arthritis, fibromyalgia) • 3. Nociceptive Pain: Caused by tissue damage (e.g., burns, cuts) • 4. Neuropathic Pain: Resulting from nerve damage (e.g., diabetes, shingles) • 5. Visceral Pain: Originating from internal organs (e.g., appendicitis, kidney stones)
  • 8.
    1. ACUTE PAIN •-Duration: Short-term, usually less than 3-6 months •- Cause: Injury, surgery, infection, or inflammation •- Characteristics: - Sudden onset •- Sharp, stabbing, or aching sensation •- Usually resolves with healing •- Example: post-operative pain, broken bone, or acute appendicitis
  • 9.
    2. CHRONIC PAIN •-Duration: Long-term, persists beyond 3-6 months •- Cause: Ongoing conditions like arthritis, fibromyalgia, or nerve damage Characteristics: •- Persistent or recurring pain •- Can be dull, aching, or burning •- Impacts daily life and mental health •Example: chronic back pain, arthritis, or fibromyalgia
  • 10.
    3. NOCICEPTIVE PAIN -Cause: Tissue damage or inflammation Characteristics: - Sharp, stabbing, or aching sensation - Usually localized to the affected area -Example: burns, cuts, fractures, or sprains- Subtypes: -Somatic nociceptive pain (skin, muscles, bones) -Visceral nociceptive pain (internal organs)
  • 11.
    4. NEUROPATHIC PAIN- •Cause:Nerve damage or dysfunction Characteristics: •- Burning, shooting, or stabbing sensation •- Can be spontaneous or triggered by stimuli •- Often accompanied by numbness, tingling, or weakness •- Example: diabetic neuropathy, shingles, or multiple sclerosis
  • 12.
    5. VISCERAL PAIN •-Origin: Internal organs (e.g., abdomen, thorax, pelvis) •- Cause: Inflammation, infection, or obstruction •- Characteristics: •- Dull, aching, or cramping sensation •- Often referred to other areas (e.g., shoulder pain from gallbladder issue) •- Example: appendicitis, kidney stones, or inflammatory bowel disease
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    1. TRANSDUCTION- • Nociceptors:Specialized nerve endings that detect tissue damage, inflammation, or other harmful stimuli • Activation: Nociceptors respond to various stimuli, such as: - Mechanical (pressure, stretch, vibration) - Thermal (heat, cold) - Chemical (inflammation, toxins) - Electrical (direct stimulation) - Signalling: Activated nociceptors release neurotransmitters, like substance P and calcitonin gene-related peptide (CGRP), which transmit signals to the spinal cord
  • 17.
    2. TRANSMISSION • -Spinal Cord: Signals from nociceptors enter the spinal cord through dorsal roots • Ascending Pathways: Signals ascend through the spinal cord via: - Spinothalamic tract (STT): transmits pain, temperature, and touch information - Spinoreticular tract (SRT): involved in pain modulation and emotional response - Spinomesencephalic tract (SMT): transmits pain information to the brainstem - Nerve Fibers: Signals travel through A-delta (A ) δ and C fibers: - Aδ fibers: fast, myelinated fibers transmitting sharp, localized pain - C fibers: slow, unmyelinated fibers transmitting dull, aching pain
  • 18.
    3. PERCEPTION • -Brainstem: Signals reach the brainstem, where they're processed and modified by various structures: • Periaqueductal gray (PAG): involved in pain modulation and emotional response • Reticular formation: regulates arousal, attention, and pain perception - Thalamus: Signals relayed to the thalamus, which acts as a sensory processing hub - Cortex: Signals reach the somatosensory cortex, where pain is perceived and interpreted: - Primary somatosensory cortex (SI): processes basic sensory information - Secondary somatosensory cortex (SII): involved in pain localization and intensity - Insula: contributes to pain emotion, empathy, and interoception
  • 19.
    • The braininterprets these signals as pain, taking into account various factors, such as: - Intensity - Duration - Location - Quality (sharp, dull, burning, etc.) - Emotional state - Past experiences - Expectations - This complex process allows us to perceive and respond to pain, enabling us to protect ourselves from harm and maintain homeostasis.
  • 20.
    3 THEORIES OFPAIN: 1. Specificity Theory 2. Pattern Theory 3. Gate Control Theory
  • 21.
    1. SPECIFICITY THEORY •Proposed by: Max von Frey (1894) • Key idea: Pain is a specific sensation with its own dedicated receptors and pathways • Assumptions: - Pain has its own unique sensory system - Nociceptors detect specific painful stimuli - Signals transmitted through specific pain pathways- • Strengths: - Explains why pain is a distinct sensation - Supports the existence of nociceptors • Weaknesses: - Oversimplifies pain processing - Doesn't account for individual differences in pain perception
  • 22.
    2. PATTERN THEORY •Proposed by: Ronald Melzack and Patrick Wall (1962) • -Key idea: Pain is a pattern of nerve activity interpreted by the brain • Assumptions: - Pain is a complex sensory experience - Nerve activity patterns are decoded by the brain - Context and past experiences influence pain perception - Strengths: - Recognizes pain's subjective nature - Emphasizes the role of brain processing - Weaknesses: - Difficult to test and quantify - Doesn't fully explain pain mechanisms
  • 23.
    3. GATE CONTROLTHEORY • Proposed by: Ronald Melzack and Patrick Wall (1965) • Key idea: Pain is modulated by the brain's ability to gate or block signals- • Assumptions: - Pain signals can be blocked or reduced by other sensory inputs - The brain acts as a "gate" controlling pain transmission - Activation of certain nerves can close the gate, reducing pain • Strengths: - Explains pain modulation and relief - Supports the use of alternative therapies (e.g., acupuncture) • Weaknesses: - Oversimplifies pain mechanisms - Doesn't fully account for individual differences
  • 26.
    PAIN MODULATION: 1. AscendingPain Modulation 2. Descending Pain Modulation 3. Segmental Pain Modulation
  • 27.
    1. ASCENDING PAINMODULATION • Signals from nociceptors transmit to the spinal cord and brain • Ascending pathways: - Spinothalamic tract (STT): transmits pain, temperature, and touch - Spinoreticular tract (SRT): involved in pain modulation and emotional response - Spinomesencephalic tract (SMT): transmits pain information to the brainstem • Brain regions involved: - Thalamus: relays sensory information - Somatosensory cortex: processes pain location and intensity - Limbic system: processes emotional aspects of pain
  • 28.
    2. DESCENDING PAINMODULATION • Brain sends signals to reduce pain transmission • Mechanisms: - Endogenous opioids (endorphins, enkephalins): natural painkillers - Opioid receptors: activated by opioids, reducing pain transmission - Monoamine systems (serotonin, noradrenaline): regulate pain modulation • Descending pathways: - Periaqueductal gray (PAG): sends signals to spinal cord to reduce pain - Reticular formation: regulates arousal and pain modulation - Rostral ventromedial medulla (RVM): sends signals to spinal cord to reduce pain
  • 29.
    3. SEGMENTAL PAINMODULATION •Local spinal cord mechanisms modulate pain •Mechanisms: - Inhibition: reducing pain transmission - Facilitation: enhancing pain transmission - Gating: controlling pain transmission- •Segmental pathways: - Dorsal horn: receives and processes pain information - Ventral horn: sends signals to muscles and glands - Spinal interneurons: regulate pain modulation
  • 30.
    SIDE NOTES: •These painmodulation mechanisms interact and coordinate to regulate pain perception. •Understanding these processes helps develop effective pain management strategies, including pharmacological and non-pharmacological interventions.
  • 31.