TRANSCUTANEOUS

ELECTRICAL NERVE
STIMULATION (TENS)
TENS
 Transcutaneous Electrical
Nerve Stimulation is the
application of low
frequency current in the
form of pulsed currents
through surface electrodes
on the patient's skin to
reduce pain.
 The effect and use of TENS
depends upon gait control
theory and pain modulation
 TENS PARAMETERS
 CURRENT INTENSITY: range of 0 - 80 mA
 FREQUENCY: From about 1 or 2 pulses per second
(pps) up to 200 or 250 pps or hz
 DURATION (OR WIDTH)OF EACH PULSE: From
about 40 to 250 micro seconds (µs)
PHYSIOLOGY OF PAIN
 Pain is an unpleasant disturbed sensation, which
accompanies the activation of nociceptors.
 Nociceptors carry noxious stimulus.
 These are free nerve endings found in all body
tissues.
 They carry pain stimulus to the higher centers.
 Once a nociceptor is stimulated, it releases a
neuropeptide, which initiates the electrical
impulses along the afferent fibres towards the
spinal cord.
PHYSIOLOGY OF PAIN
 These afferent fibres are of two types:
 A Delta fibres:
Fast conducting small diameter
myelinated fibres, which conduct with a
velocity of 5-30 m/s.
 C fibres:
Slow conducting small diameter non-
myelinated fibres, which conduct with a
velocity of 2-5 m/s.
 First order or primary afferent fibers
transmit impulses from the sensory
receptors to the dorsal horn of the spinal
cord. Second order afferent fiber carry
sensory impulses from the dorsal horn of
the spinal cord to the brain
 First order neurons include A- alpha, A-
beta, A- delta and C- fibers. A- alpha and
A- beta fibers are characterized by having
large diameter afferents
PHYSIOLOGY OF PAIN
Pain Gate Theory
 Under normal physiological circumstances, the
brain generates pain sensations by processing
incoming noxious information arising from stimuli
such as tissue damage.
 In order for noxious information to reach the brain
it must pass through a ‘pain gate’ located in lower
levels of the central nervous system.
 In physiological terms, the gate is formed
by excitatory and inhibitory synapses
regulating the flow of neural information
through the central nervous system.
 This ‘pain gate’ is opened by noxious
events in the periphery
PAIN GATE
THEORY
PHYSIOLOGY OF PAIN
 The pain gate can be closed by activation of
mechanoreceptors through ‘rubbing the skin’.
 This generates activity in large diameter Aβ
afferents, which inhibits the onward transmission of
noxious information.
 This closing of the ‘pain gate’ results in less noxious
information reaching the brain reducing the
sensation of pain.
 The aim of conventional TENS is to activate Aβ
fibres using electrical currents
PHYSIOLOGY OF PAIN
 The pain gate can also be closed by the activation
of pain-inhibitory pathways which originate in the
brain and descend to the spinal cord through the
brainstem (extrasegmental circuitry).

 These pathways become active during psychological

activities such as motivation and when small
diameter peripheral fibres (Aδ) are excited
physiologically
MECHANISM OF ACTION OF TENS
 The type of stimulation delivered by the
TENS unit aims to excite (stimulate) the
sensory nerves, and by so doing, activate
specific natural pain relief mechanisms.

 Gait Control Theory/ Pain Gate Theory

 Pain Modulation
MECHANISM OF ACTION OF TENS
 Pain relief by means of the
pain gate mechanism involves
activation (excitation) of the A
beta (Aβ) sensory fibres, and
by doing so, reduces the
transmission of the noxious
stimulus from the ‘C’ fibres,
through the spinal cord and
hence on to the higher centres.
 The Aβ fibres appear to
appreciate being stimulated at
a relatively high rate (in the
order of 90 - 130 Hz or pps
MECHANISM OF ACTION OF TENS
 An alternative approach is to stimulate the A
delta (Aδ) fibres which respond
preferentially to a much lower rate of
stimulation (in the order of 2 - 5 Hz),

 Which will activate the opioid mechanisms,

and provide pain relief by causing the
release of an endogenous opiate (encephalin)
in the spinal cord which will reduce the
activation of the noxious sensory pathways.
MECHANISM OF ACTION OF TENS
MECHANISM OF ACTION OF TENS
 Neurophysiology of
AL-TENS analgesia.
 Activity in Aδ and C
fibres from
nociceptors leads to
excitation (+) of
central nociceptor
transmission neurons
(T) which project to
the brain to produce
a sensory experience
of pain
MECHANISM OF ACTION OF TENS
 TENS-induced activity in small diameter
muscle afferents (Aδ, GIII) leads to the
activation of brainstem nuclei such as the
periaqueductal grey (PAG) and nucleus raphe
magnus (nRM).

 These nuclei form the descending pain

inhibitory pathways which excite
interneurons which inhibit (−) SG and T cells
(dotted line) via the release of enkephalin
TYPES OF TENS
High TENS or Brief Intense TENS:
 In this high frequency and low intensity electrical
stimulation is applied.
 The stimulation will cause impulse to be carried along
with the large diameter afferent fibers (Aβ) and
produces pre-synaptic inhibition of transmission of
nociceptive A-delta and C fibers at susbstantia
gelatinosa of the pain gate.
 Frequency 100-450 Hz
 Pulse Width 100 and 500ms
 Intensity 12-30mA,
TYPES OF TENS
High TENS or Brief Intense TENS:
 More effective in acute pains
 Can be used for as long as needed
 Minimum Time: 15-30 mins
TYPES OF TENS
Low TENS or Acupuncture TENS (ACUTENS)
 Low frequency and high intensity electrical
pulses are applied, gives a sharp stimulus
and like a muscle twitch.
 Activates Aδ Fibres, => Opioid system
activation => Relieve pain
 Frequency 1-5Hz
 Pulse Width 100 and 500ms
 Intensity 30mA or more
 30 mins Minimal effect dose
TYPES OF TENS
Low TENS or Acupuncture TENS (ACUTENS)
 More effective in chronic pains
 Can be used as long as needed but commonly used in
STIM/REST pattern (1-2 hr ON followed by 1-2 hr OFF)
TYPES OF TENS
Burst Mode TENS
 The higher frequency stimulation output (typically at
about 100Hz) is interrupted (or burst) at the rate of
about 1 - 5 bursts per second.
 When the machine is ‘on’, it will deliver pulses at the
100Hz rate, thereby activating the Aβ fibres and the
pain gate mechanism, but by virtue of the rate of the
burst, each burst will produce excitation in the Aδ
fibres, therefore stimulating the opioid mechanisms.
 It is proposed that the application of BURST mode TENS
can effectively stimulate both the PAIN GATE and the
OPIOID mechanisms simultaneously
METHODS OF TREATMENT
Placement of electrodes
 Area of greater intensity of pain.
 To the appropriate dermatome.
 Superficial nerve proximal to the site of pain in case of
Phantom limb pain
 Contra-lateral to the site of pain in conditions such as
phantom limb pain and trigeminal neuralgia where the
affected side of the face may be sensitive to touch
 To the nerve trunk
 Trigger point
METHODS OF TREATMENT
Placement of electrodes
 TENS can be used with single
channel of electrodes or
doubled channeled
 Vertical placement
 Horizontal placement
 Criss-cross placement

Vertical placement
 Apply one channel of
electrodes to the right side
and one channel to the left
side
METHODS OF TREATMENT
Horizontal placement
 Apply one channel above
the area to be treated
and one channel below

Criss-cross placement
 Connect the leads to the
electrodes so that one
channel crosses the other
channel
MOTOR POINTS UPPER LIMB
MOTOR POINTS LOWER LIMB
MOTOR POINTS FACE
INDICATIONS FOR USE
 TENS can be used for the treatment of:
 Chronic pain syndrome.
 Phantom limb pain.
 Reflex sympathetic dystrophy.
 Post operative pain.
 Obstetric pain.
DANGERS AND
CONTRAINDICATIONS
 Continuous application of high TENS may result
in some electrolytic reaction below the skin
surface.
 TENS is contraindicated in patients having
cardiac pacemakers may be because of possible
interference with the frequency of pacemaker.
 TENS should be avoided in first three months of
pregnancy.
 TENS should be avoided in hemorrhagic
conditions.
 TENS should be avoided over open wounds,
carotid sinus, over the mouth, near eyes, etc