TENS lecture learning aims:
1. be able to describe the basic physiological mechanisms of pain modulation
More specifically you will…
2. be able to describe how a nociceptive signal is affected by therapeutic modalities, i.e.
Transcutaneous Electrical Nerve Stimulation (TENS).
3. be able to describe the traditional gate control theory of pain (‘pain gate’) and
why current thinking has changed
4. be able to describe the descending pain suppression theory / endogenous opioid system
5. be able to apply this knowledge to guide TENS settings
TENS parameters:
Frequency – how often the pulses are (pulse per second)
amplitude – how tall the spikes are (strength) the patient decides this, they need to put what
they can tolerate.
Pulse width – how long does the pulse stay (pulse duration)
Duration – how long the patient will have the TENS on
Low intensity Vs. High Intensity
Low Intensity High Intensity
(Traditional or (Acupuncture)
Conventional) TENS TENS
FREQUENCY >85hz (90-130hz) 1- 4hz (2-5hz)
AMPLITUDE Low mA High mA
PULSE WIDTH 50-80 μs 200 μs
DURATION 30 mins 30 mins
, Production of nociceptive signal
• Tissue damage
• Mechanical (e.g. crushing, tearing, shearing)
• Thermal (e.g. heat or cold)
• Chemical
• lack of oxygen (i.e. lack of blood supply – ischaemia)
• Tissue damage releases histamine (released from mast cells and basophils (a class of
white blood cells).
• Mast cells degranulate (i.e. breakdown) and release histamine (and serotonin)
• Mast cells live in the connective tissue.
1. Histamine stimulates/irritates the nociceptors AND lowers the threshold for production
of a nociceptive signal.
2. Histamine triggers the inflammatory response
• Triggers the release of other inflammatory mediators such as, bradykinin
and prostaglandin.
3. Histamine increases the permeability of the capillaries to white blood cells and proteins
• This allows the other inflammatory mediators to gather at the site of
injury.
4. Histamine triggers the release of substance P in the periphery and at the spinal cord as
a neurotransmitter
• Sensitizes the nociceptor (primary sensitization) and increases the rate of
firing.
• The nociceptor transforms the chemical stimuli into an electrical signal.
Signal goes into the dorsal area of the spinal cord.
Nociceptive nerve fibres –
A delta fibres
• ‘fast’ - conduct action potentials rapidly
• axons are myelinated.
• Signals perceived as ‘sharp’ pain (fast/first pain sensations)
• respond to extremes of heat, cold and mechanical stimuli
• generates withdrawal reflex
C fibres
• ‘slow’.
• conduct slow action potentials.
• Un-myelinated axons
• signals perceived as ‘aching or burning’ (slow/second pain sensations)
• responds to noxious thermal, mechanical and chemical stimuli released during cell
damage.
1. be able to describe the basic physiological mechanisms of pain modulation
More specifically you will…
2. be able to describe how a nociceptive signal is affected by therapeutic modalities, i.e.
Transcutaneous Electrical Nerve Stimulation (TENS).
3. be able to describe the traditional gate control theory of pain (‘pain gate’) and
why current thinking has changed
4. be able to describe the descending pain suppression theory / endogenous opioid system
5. be able to apply this knowledge to guide TENS settings
TENS parameters:
Frequency – how often the pulses are (pulse per second)
amplitude – how tall the spikes are (strength) the patient decides this, they need to put what
they can tolerate.
Pulse width – how long does the pulse stay (pulse duration)
Duration – how long the patient will have the TENS on
Low intensity Vs. High Intensity
Low Intensity High Intensity
(Traditional or (Acupuncture)
Conventional) TENS TENS
FREQUENCY >85hz (90-130hz) 1- 4hz (2-5hz)
AMPLITUDE Low mA High mA
PULSE WIDTH 50-80 μs 200 μs
DURATION 30 mins 30 mins
, Production of nociceptive signal
• Tissue damage
• Mechanical (e.g. crushing, tearing, shearing)
• Thermal (e.g. heat or cold)
• Chemical
• lack of oxygen (i.e. lack of blood supply – ischaemia)
• Tissue damage releases histamine (released from mast cells and basophils (a class of
white blood cells).
• Mast cells degranulate (i.e. breakdown) and release histamine (and serotonin)
• Mast cells live in the connective tissue.
1. Histamine stimulates/irritates the nociceptors AND lowers the threshold for production
of a nociceptive signal.
2. Histamine triggers the inflammatory response
• Triggers the release of other inflammatory mediators such as, bradykinin
and prostaglandin.
3. Histamine increases the permeability of the capillaries to white blood cells and proteins
• This allows the other inflammatory mediators to gather at the site of
injury.
4. Histamine triggers the release of substance P in the periphery and at the spinal cord as
a neurotransmitter
• Sensitizes the nociceptor (primary sensitization) and increases the rate of
firing.
• The nociceptor transforms the chemical stimuli into an electrical signal.
Signal goes into the dorsal area of the spinal cord.
Nociceptive nerve fibres –
A delta fibres
• ‘fast’ - conduct action potentials rapidly
• axons are myelinated.
• Signals perceived as ‘sharp’ pain (fast/first pain sensations)
• respond to extremes of heat, cold and mechanical stimuli
• generates withdrawal reflex
C fibres
• ‘slow’.
• conduct slow action potentials.
• Un-myelinated axons
• signals perceived as ‘aching or burning’ (slow/second pain sensations)
• responds to noxious thermal, mechanical and chemical stimuli released during cell
damage.
