Pain & Healing

• Chronic

  Injury caused by prolonged exposure to repetitive stress
• Chronic phase of healing


  Remodelling or maturation phase. Phase of healing where the tissue re-organizes to meet the demand placed upon it
• Chronic pain

  Pain that persists beyond the structural dysfunction. I.e. The tissue integrity is within normal limits, but the pain experience persists. Maladaptation of the injury (mediated via the nervous system)
• Chronic pain is not to be confused with persisting pain or prolonged pain (poor healing)
• Myths about pain

  • Simple stimulus-response mechanism
  • Directly related to the severity of trauma
• Reality of pain

  • Biopsychosocial factors modulates pain responses
  • Psychological state at the time of injury
  • Context of injury
• Pros of pain

  • Its main purpose is good; it protects you by alerting you to danger and stimulating action that prevents or minimizes injury
  • Pain serves as a warning for withdrawal
  • Pain alerts a person that something is wrong
  • Pain protects the injured part of the body through muscle guarding (muscle spasm)
• Cons of prolonged or chronic pain

  • Disability
  • Atrophy, circulatory deficiency
  • Loss of skill
  • Anxiety and depression
  • Marked decrease in the quality of life
  • Decreased activity
  • Deconditioning
• Types of noxious stimuli

  • Mechanical stimulus: Stimulation caused by pressure on a nerve, often due to swelling or muscle spasm
  • Thermal stimulus: Stimulation caused by radiant heat, such as the ultraviolet rays of the sun or a burn from touching a hot object
  • Electrical stimulus: Touching a "hot" wire and feeling the "buzz" from poor grounding of a light socket are examples of mild electrical stimuli
  • Chemical stimulus: During the inflammatory response, chemical mediators transmit pain through the body to alert you that something is wrong. One of these chemicals is bradykinin, probably the most painful substance known
• Pain pathway- simplified

  1. Noxious stimuli initiates a pain signal in the injured toe that travels as an electrochemical impulse along a first-order neuron up the entire length of the leg to the Dorsal horn of the spinal cord

  2. The impulse then synapses with the second-order neuron and is then relayed up the spinal cord (spinothalamic tract) to the thalamus and then synapses with the third-order neuron and travels to the cerebral cortex
• First-order neurons

  Transmit sensory information from the receptor to the dorsal horn of the spinal cord
• Second-order neurons

  Transmit information from sensory pathways and various reflex networks in the spinal cord to the thalamus
• Third-order neurons

  Relay information from the thalamus to the cerebral cortex
• The three orders of sensory neurons correspond to the three levels of neural integration; sensory reception, ascending pathways, and central processing
• The spinal cord consists of thousands of individual nerve fibers. Some fibers are covered with myelin, a white insulating substance that makes areas appear white. In the spinal cord, the white matter is myelinated axons. The gray matter is unmyelinated axons, plus neuron cell bodies and dendrites. The pattern of the four areas of unmyelinated fibers makes the gray matter appear to have horns. The dorsal horns are the two horns at the posterior side of the cord. The ventral horns are the two horns at the anterior side. Afferent nerves enter the spinal cord via the dorsal horns, and efferent nerves exit the spinal cord via the ventral horns
• Nociceptive pain


  Occurs in response to injury or illness to bodily structures. It involves messages conducted from nociceptors at the site of injury, on efferent nerves up through the spinal cord into the brain, where the messages are interpreted as pain
• Neuropathic pain


  A complex, chronic pain state that often shows up in illogical ways. It usually is accompanied by tissue damage to the nerve fibers themselves. Thus the nerve fibers become dysfunctional and send incorrect signals to the brain and other pain centers
• Idiopathic pain


  Pain of unknown origin, meaning there is no identifiable pathology associated with it
• Learned pain

  A phenomenon that develops from a patient's "pain memories" of physiological and emotional elements of either a nociceptive or neuropathic pain experience. One explanation is that following a specific pain-producing stimulus, such as injury, organic disease, or surgery, the pain stimulus is indirectly paired with any of an infinite number of environmental or sociologic stimuli, even inactivity. In time, pain can be elicited by the secondary stimuli, and thus becomes a learned—or conditioned—response, via the classic pavlovian conditioning of dogs to salivate when they heard the ringing of a bell
• 3 levels of pain control

  • Ascending Influence Pain Control: Pain relief induced by a gating mechanism occurs during the application of modalities such as traditional TENS, massage, and cryotherapy
  • Descending Influence Pain Control: Pain relief modulated by transmissions from higher brain centers, such as in the RN (red nuclei) to the dorsal horn of the spinal cord, which triggers the release of enkephalin and modulates pain
  • Beta-Endorphin-Mediated Pain Control: Prolonged stimulation of afferent nerves (A-delta fibers) triggers the release of beta-endorphin by the pituitary gland from connections between the hypothalamus and the RN. Since beta-endorphin has a long half-life, this provides long-term stimulation of descending tracts
• Gate control theory

  A model of the three main aspects: (1) Both large-diameter and small-diameter afferent nerve fibers facilitate the T cell, which transmits the signal to the action system. (2) A group of cells in the substantia gelatinosa (SG) of the dorsal horn constantly send inhibitory signals to the T cell. SG cells are facilitated by large sensory nerves and inhibited by small sensory nerves. (3) Central control, located in the brain, can either facilitate (+) or inhibit (-) T-cell transmission. Central control receives signals from both large and small fibers
• Operating at the spinal level, the gate control theory proposed that a gating mechanism, located in the dorsal horn of the spinal cord, allows only one sensation at a time to pass through to the brain. The theory recognized that pain and other sensory stimuli travel along both large-diameter and small-diameter nerve fibers, which converge at the T cell (transmission cell), which is the gate. The T cell determines which impulse will continue up or down the spinal cord and subsequently to other parts of the body (the action system) where various actions will be invoked
• Sharp, stinging pain travels along large fibers, whereas dull, aching pain travels along small fibers. Other sensations also travel along both fiber types. Strong sensory stimulation can control pain by "closing the gate" to pain, as the gate (the T cell) opens to allow the stronger sensory stimuli to pass through to the action system
• Another aspect of the gate control theory is an inhibitory mechanism located in the substantia gelatinosa (SG) [tract] in the dorsal horn of the spinal cord. The SG sends inhibitory interneurons to the T cell. It is always active, constantly providing self-generated background inhibition to the T cell. In addition to its self-generated inhibition, the SG is influenced by stimuli from both large and small fibers via interneurons. The two types of fibers have different effects on the SG and therefore modify the inhibition the SG exerts on the T cell. Large-fiber stimulation facilitates the SG, thus increasing its inhibition on the T cell. Small-fiber stimulation, however, inhibits the SG, thereby decreasing the inhibition the SG has on the T cell
• Descending endogenous opiate theory

  The descending endogenous opiate system (DEOS) is illustrated on the right. The gate control, on the left, is shown for comparison
• Central control trigger theory

  A modification of the gate control theory. It involves the original gating mechanism plus an additional central inhibitory mechanism. The former modulates the T-cell neurons as originally proposed (i.e., central control) and the latter acts via endorphin and enkephalin. Thus, there are at least two different mechanisms of pain control in the spinal column, one local and one via descending tracts
• Soft Tissue healing phases

  • Inflammatory phase
  • Proliferative phase
  • Maturation phase
• Inflammatory phase

  1. Immediate response (24-48 hours)

  2. Primary and secondary tissue injury

  3. Primary injury: Initial mechanical trauma and cell damage

  4. Secondary injury: Inflammatory cascade
• Cardinal signs and symptoms of inflammation

  • Redness
  • Swelling
  • Heat
  • Pain
  • Loss of function
• Primary and secondary injury

  1. Mast cells are the first activated. Sit in the capillary bed with WBCs, they release histamine and bradykinin that causes vasodilation, increasing permeability, creating swelling (histamine and bradykinin = pain)

  2. Arterioles vasodilate engorging the capillaries, which separates the endothelial cells which further increases permeability (swelling). The compression caused by accumulation of fluid decreases oxygen

  3. Chemotaxis means cell signaling (mast cells are chemotactic to WBC)

  4. WBC=neutrophils and monocytes =phagocytes

  5. Neutrophils are microphages and destroy anything they come in contacts with

  6. Monocytes only clear out dead debris

  7. Hypoxia and phagocytosis = secondary injury
• Inflammation is necessary to the healing process, but swelling and hemolytic changes create a secondary metabolic injury that can increase the severity of the injury (tissue damage)
• Ice can be applied to help with the inflammatory response
• Proliferative (repair) stage

  1. Phagocytosis: clean up dead cells and debris (WBC)

  2. Fibrinolysis: break down of blood clot

  3. Angiogenesis: capillary sprouting (increase O2)

  4. Wound contraction: closing/shrinking

  5. Fibrosis

  6. Fibroplasia: fibroblasts migrate to the damaged area (collagen synthesis and deposit)

  7. Scar formation: laying down and organizing of collagen in ground substance (extracellular matrix)
• Maturation (remodeling) phase

  1. Scar tissue begins forming 3-4 days post injury

  2. Scar formation may take months, and never reaches strength of pre-injury tissue

  3. Collagen maturation: re-organization of collagen is an on-going remodeling process

  4. Tensile strength of scar is proportional to: Density of collagen fibers, Orientation of fibers (parallel)
• Davis's law

  Soft tissue adaptation to imposed demands. Mechanical loading response adaptive change hypertrophy increased tissue strength. Basis for designing sport-specific rehab programs
• Bone healing types

  • Primary bone healing: Involves a direct attempt by the cortical bone to re-establish itself after interruption without the formation of a fracture callus. Not common naturally- usually from surgical fixation
  • Secondary bone healing: New bone is deposited to fill in the gap. Goes through similar steps of healing as soft tissues
• Reactive stage of bone healing

  1. Lasts about 2-4 days

  2. Fracture hematoma (blood clot)
• Reparative stage of bone healing

  1. Within 7-10 days, a soft callus (pro-callus) will fully replace the hematoma

  2. Granulation tissue (fibroblasts and new blood vessels (angiogenesis))

  3. The fibroblasts produce cartilage cells

  4. In 4-6 weeks, the soft callus will transform into a hard callus

  5. Substitution of fibrocartilage with spongy bone (ossification)

  6. 2 types: Intramembranous (girth): Margins of the bone such as the periosteum, Endochondral (internal)

  7. Milestone for repair: Radiographic union (can see the hard callus on x-rays)
• Remodeling Stage of bone healing

  1. 6 weeks to months

  2. Internal and external calluses unite

  3. Re-organization of fibers according to Wolff's Law