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TENS Transcutaneous electrical stimulation - Coggle Diagram
TENS
Transcutaneous electrical stimulation
What is TENS?
Method of electrical stimulation
↓ pain by exciting sensory nerves and thereby stimulating either the
pain gate mechanism and/or the opioid system
The different methods of applying TENS relates to these different physiological mechanisms
Treatment for chronic pain- less evidence for acute pain
non-invasive & has few side effects
Most common complaint is an allergic type skin reaction due to the material of the electrodes, gel or tape to hold electrodes
Pulse Width settings
This is when the pulse width is 'on'
measured in microseconds (uS)
Generally recommend: 175 to 200uS
TENS settings
Pain gate (conventional)
High frequency, low intensity
Descending Inhibition - endogenous opioids (acupuncture-like TENS)
Low frequency, High intensity
Burst TENS
Series of pulses every 1-5 seconds
How to do TENS?
Explanation to patient
Input settings to unit
Electrode placement- red nearest head
Place on over the area of pain and one distally
Turn on machine till a strong comfortable sensation is felt
Turn up machine as nerves accommodate
Modes of TENS settings
Normal
-constant stimulation- most often for acute pain relief via pain gate
Modulation
- frequency varies to help reduce nerve adaptation (useful for acute & chronic pain)
Burst-
the unit will send through burst of pain relieving power (useful for chronic pain)
Frequency of TENS settings
- Acute Pain
= 80-100Hz
- Chronic Pain
= 2-10Hz
How long to use for?
Acute pain
- 20 minutes-60 minutes (up to x4 a day)
Chronic pain
- 20 minutes - 60 minutes (up to x5 per week)
Contraindications
Patients who do not comprehend the physiotherapists instructions or who are unable to co-operate
Patients who have a allergic response to the electrodes, gel or tape
Patients who have a pacemaker shouldn't be routinely treated
Electrodeplacement over dermatological lesions. eczma
Application over anterior aspect of neck or carotid sinus
Pain gate therory
Melzack and wall (1965) explains that non-painful input closes the nerve gate to painful input and prevents pain sensation from reaching the CNS
This is done by the stimulation of large myelinated fibres such as a-alpha and a-beta.
Dueto the myelin they are faster than a-delta and c nerve nociceptors that causepain. The impulses reach the dorsal horn before the noxious (painful) stimuli the inhibitory neurone is stimulated and acts as a gate and blocks the pain signal from the projector neurone from reaching the brain
Descending Inhibition- endogenous opioids
In the CNS there are 3 opioid receptors which regulate the neurotransmission of pain signals.
They are G protein-coupled receptors
Their activation leads to a reduction in neurotransmitter release and cell hyperpolarisation, reducing cell excitability.
Our body contains endogenous opioids which can modulate pain physiologically
3 typesof endogenous opioids
B-endorphins- binds to mu opioid receptors
Dynorphins- binds to kappa opioid receptors
Enkephalins- bind to delta opioid receptors
opioids reduce pain transmission at the dorsal horn by inhibiting excitatory neurotransmitter release