Lecture 6: Hot and Cold Flashcards
Pain
Unpleasant sensory and emotional experience associated with actual or potential tissue damage
Pain receptors
Nociceptors
sensitive to mechanical (tearing), thermal, chemical
afferent nerve fibres carry info from nociceptors to spinal cord
Types of Pain Signals
A delta (myelinated) = fast pain
C fibres (UNmyelinated) = slow pain
A delta fibres
- myelinated + large diameter = fast pain
- touch, pressure and temp
- located in skin
- ex. hand in alligator’s mouth or hand on stove (tells to move hand right away)
C fibres
- unmyelinated + small diameter = slow pain
- pain and temp
- located skin and deep tissue (muscle/lig)
- reminder that you’re sore
Gate Control Theory of Pain (no stimulation)
Without stimulation, A beta (large) + C (small) fibres are quiet
- SG and inhibitory interneuron block signal in T cell
- gate is closed = NO pain
Substantia Gelatinosa
Transfer station or volume control
- located in dorsal horn of lateral spinothalamic tract
Blocks pain by increasing signals from inhibitory interneuron to block C fibre signals from getting to T cell and feeling pain
Gate Control Theory of Pain (pain stimulation)
With pain stimulation, C fibres are active and BLOCK inhibitory SG and activate T cells
- inhibitory interneuron is blocked = CANNOT block output of T cell
- gate is open = PAIN
Gate Control Theory of Pain (non-painful stimulation)
With non-painful stimulation, A beta (large) fibres are activated
- activates SG = activation of inhibitory interneuron = BLOCKS signal in T cell
- gate is closed = NO pain
What fibres do we want to block? What do we not want to block?
Want to decrease C-fibre pain b/c it’s leftover pain
NEVER want to block A-delta pain b/c it protects us
A-beta fibres
Blocks C fibre input
- responds to pressure, vibration, position sense
Pressure: rubbing head when you bump it, massage
- stimulates A-beta input = increase in SG = block C fibre
Vibration: 4 Hz taps on ankle x 10 min = released opiates and closed gate
Position sense: shaking finger, AROM/PROM
Fibre accommodation
Accommodation = rise in threshold
- if a nerve shows constant strength of current, site of nerve has lower excitability
Constant input = no sensation to body
- A fibres will accommodate (A-beta fibres will be ignored and pain starts again)
- C fibres will NOT accommodate
Cold and Superficial Heat
- therapeutic modalities
- conduct heat to or away from the body
- applied to speed up healing… evidence?
- may cause injury if used improperly
- cold = cryotherapy, heat = thermotherapy
Cold and blood flow
- Spinal cord: decrease in blood flow in 1st 5-15 mins
- Local/superficial: oscillations
- reflex vasodilation/constriction to try to reheat cold area - Hypothalamus (linear level of cold)
go from 1 to 3 as time increases
Body’s response to cold depends on…
- cold media being applied (ice, cold water immersion)
- conductivity of area being cooled
- high water content in tissue = less cooling
- muscle > fat
- joints > muscle (b/c of synovial fluid) - Length of time of exposure
- longer is not always better
- Bleakley et al.: 10 on- 10 off - 10 on
Bleakley et al
Explained that ice should be used in this way: 10 on/10 off/10 on (superior to 20 mins on)
avoids vasodilation/vasoconstriction reflex that causes blood flow to be pushed to area to rewarm cool skin (stays cold)
What happens w/ acute injuries?
- tissue injury at primary + secondary sites = cell death due to hypoxia
- increased bleeding into area
- pain
- swelling/edema
Body’s physiological responses to cryotherapy
- decrease in muscle guarding = breaks pain/spasm cycle
- decrease blood flow
- decrease capillary permeability
- decreased O2 required= less secondary injury
- decreased collagen elasticity
- increased joint stiffness
- decreased pain perception (C fibre conduction rate drops)
- edema is controversial (does not reduce current swelling but might reduce future swelling)
Metabolic rate and cryotherapy
When injured, blood flow is reduced and can lead to cell death from hypoxia
Ice decreases metabolism of cells = less O2 is needed
- O2 provided after injury is now enough to survive
Case AGAINST ice use
- inflammatory/destruction phase of healing is necessary
Evidence that ONE early ice treatment may slow down healing over first 3-7 days (impaired tissue repair)
- more necrosis in ice group at day 3
- less neutrophils day 1 and more day 3 in ice group
- less macrophages at day 1 and 3 w/ more at day 7 in ice group = delayed inflammation
Case FOR ice use
Good for pain
- C fibres are not myelinated
- every 1 degree drop in temp = decreasing conduction velocity of a nerve
- 4 degree cooling = C fibres knocked out
Combined w/ exercise = better ability to decrease swelling compared to heat
- significant improvement in function
Maintaining cell viability after injury
- drop in chemical reactions + drop in ATP demand = drop in cellular collapse (anti-oxidant)
- don’t need as much of these things since we won’t get them either way
Body’s response to heat depends on…
- Type of heat applied
- moist heat (better for deep tissues)
- dry heat (better tolerated)
- ultrasound (mechanical) - Intensity of heat energy (some ppl are more sensitive)
- Duration of application
- blood flow until heat source is removed
- will peak 6-8 mins (body protects from getting too hot)
- when heat source is removed, tissue temp drops
Blood flow with cryotherapy and thermotherapy
Cryotherapy: variable blood flow (increases and decreases w/ oscillations)
Thermotherapy: increases then plateaus and stays constant to prevent tissue from getting too hot
Physiological responses to thermotherapy
- increased blood flow
- increased capillary permeability
- increased metabolic rate (good b/c we want to increase blood flow to area)
- increased collagen elasticity
- decreased jt. stiffness
- decreased spasm (ischemic)
- decreased pain
- edema depends on timing of heat
