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PHYSIOLOGICAL
EFFECTS OF IFT
BY: DR. LAKSHMI PAVANI P. (PT)
INTERFERENTIAL CURRENT
 Is essentially a medium-frequency current (normally approximately 4000 Hz)
 Rhythmically increases and decreases in amplitude at low frequency (adjustable between
0 & 200-250 Hz)
 Produced by mixing two low frequency currents that are slightly out of phase, either by
applying them so that they ‘interfere’ within the tissues , or alternatively by mixing them
within the stimulator prior to application (pre-modulated current)
PHYSIOLOGICAL EFFECTS OF IFT
Analgesic effects :
 The ‘pain-gate’ theory.
 Descending pain suppression
 Physiological block of nerve conduction
 placebo
Other effects:
 Muscle stimulation
 Increased blood circulation
 Edema reduction
 Placebo
PAIN TRANSMISSION
NOCICEPTORS
 Sensory receptors located at free endings of Aδ and C fibers
 Detect noxious stimuli
 Carried to the CNS
 Found in skin, viscera, muscles, joints, and meninges
 They are stimulated by the inflammatory mediators released by the damaged tissue eg:
bradykinins
SKIN NOCICEPTOR TYPE OF STIMULI
Aδ MECHANOSENSITIVE MECHANICAL
Aδ MECHANOTHERMAL THERMAL
C POLYMODAL MECHANICAL, THERMAL,
CHEMICAL
PRIMARY AFFRENT FIBERS
 Nerves that carry input from the periphery to the spinal cord.
 3 types: Aβ, Aδ and C fibers
FIBRE TYPE STIMULI ACTIVATION
THRESHOLD
DIAMETER MYELINATION TRANSMISSIO
-N
Aβ NON-NOXIOUS LOW LARGEST HIGH RAPID
Aδ NOXIOUS, RAPID,
SHARP,
LOCALISED PAIN
HIGH AND
LOW
SMALL MODERATE QUICK (but
not as fast as
Aβ)
C NOXIOUS, SLOW,
DULL, NON-
LOCALISED PAIN
HIGH SMALLEST LOW VERY SLOW
TRANSMISSION IN THE DORSAL
HORN
 Dorsal horn a.k.a Posterior column
 Grey matter within the posterior horns of spinal cord
 Primary afferent nerves release the excitatory neuro-transmittors
 Secondary afferent neurons synapse with Aδ and C fibers
 Activity of secondary neurons is affected by the activity of the afferent
neurons, interneuron and efferent neuron pathways.
ASCENDING THE SPINAL CORD
 2 main pathways carry nociceptive signals up the spinal cord to the brain.
a) spinothalamic tracts
b) spinoreticular tracts
 Pain processing in the brain
a) thalamus
b) primary and secondary somatosensory cortex
c) prefrontal cortex
INHIBITING THE PAIN TRANSMISSION
1) GATE CONTROL THEORY
2) DESCENDING INHIBITORY PATHWAYS
3) PHYSIOLOGICAL BLOCK OF NERVE CONDUCTION
1) GATE CONTROL THEORY
 Melzack and wall -1965
 Inhibition at spinal cord level / pre synaptic inhibition
Eg: Rubbing your head after bumping it
Activates Aβ fibers
Activates inhibitory interneurons
Inhibits pain transmission by C fibers
 Transmission cell- ‘T’ in dorsal horn which prefers mechanoreceptor information rather
than nociceptor information.
 Nociceptive fibers i.e Aδ and C fibers relay in the more superficial lamina i.e say lamina 1
of the dorsal horn + areas of substantia gelatinosa.
IMPULSES FIRE ON THE
POLYSYNAPTIC
INTERNEURONS
PROGRESS TO THE
HIGHER CENTERS BY THE
SPINOTHALAMIC TRACT
TO THE THALAMUS AND
THEN THE PARIETAL
LOBE
POLYSYNAPTIC INTERNEURONS
 They are cell bodies with dendrites present in the grey matter of the spinal
cord. (present in the dorsal horn too)
 Responsible for evoking motor response
Eg: when we suddenly step on a thorn
Sensory response- knowing that there was pain, location of the pain
Autonomic response- HR, RR
 Mechanoreceptors – rely on the polysynaptic interneurons in the deeper lamina of the dorsal
horn and synapse with the spinocerebellar tract/ dorsal columns.
 When there is increase in the mechanoreceptor activity, signals from the polysynaptic
interneurons are not only transmitted to the spinothalamaic tract and dorsal column, but also
fire back into the areas of Lamina 1 where the nociceptors usually fire.
 Leading to a block in the polysynaptic interneurons in the nociceptor Lamina no pain
conduction pre synaptic inhibition.
2) DESCENDING INHIBITORY
PATHWAYS
 Electrical stimulation of the periaqueductal grey matter (PAG) area can
produce analgesia, demonstrated through electrophysiological and
pharmacological studies that ‘descending influences’ on spinal nociceptive
processing involves the PAG and the Rostral Ventromedial Medulla (RVM)
(Fields, Milan -1960)
(Dorsal root ganglion
Periaqueductal grey
matter
Rostral ventromedial medulla
(Dorsal
horn)
(Nucleus Raphe
magnus)
Incoming painful stimuli are transmitted
to the dorsal horn
to the raphe nuclei, especially the nucleus raphe magnus, in the upper medulla
to the periaqueductal grey (PAG).
Descending impulses pass back Rostral ventromedial medulla (RVM)
to the dorsal horn via reticulospinal fibers.
 The periaqueductal grey matter (PAG) and the rostral ventromedial medulla (RVM)
contain high levels of opioid receptors
 Inhibition of the pain pathway occurs monoaminergically, releasing inhibitory
neurotransmitters at the spinal level. (Goats 1990, Rennie 1988)
 i.e through mono amine nerve transmitters – Nor adrenaline, dopamine, serotonin – also
known as catecholamines.
 Resulting analgesia may be long lasting , but pain may initially increase owing to the
stimulation of nociceptive Aδ and C fibers (Goats,1990)
 Post synaptic inhibition/ descending pain inhibition.
3) PHYSIOLOGICAL BLOCK OF NERVE
CONDUCTION
 Stimulation of peripheral nociceptive fibers at rates above their maximum
conduction frequency may cause cessation of action potential propagation
(De Domenico, 1982; Goats,1990; Low and Reed,2000; Rennie 1988;
Shafshak, El-Sheshai and Soltan, 1997), caused by increased stimulation
threshold and synaptic fatigue (Goats,1990)
OTHER EFFECTS
1) MUSCLE STIMULATION:
 Stimulation of the motor nerves can be achieved with a wide range of
frequencies. Clearly, stimulation at low frequency (e.g. 1Hz) will result in a
series of twitches, whist stimulation at 50Hz will result in a tetanic
contraction. (Low And Reed; shafshak,El-Shehai and Soltan,1991)
2) INCREASED CIRCULATION & EDEMA REDUCTION
 Interferential current has been claimed to improve the circulation of blood and swelling,
which may wash away the chemicals that stimulate nociceptive nerve endings (De
Domenico, 1982; Goats,1990; Rennie 1988; Shafshak, El-Sheshai and Soltan, 1991)
 Reduced swelling may concomitantly reduce tissue pressure. These phenomena are
reported to occur because of mild muscle contraction or action on the autonomic
nervous system, decreasing the tone of blood vessels ( Low and Reed; Shafshak,El-
Sheshai and Soltan,1991)
3) PLACEBO:
 Placebo responses have been identified in the literature as a potential factor with IC
stimulation (De Domenico,1982;Goats,1990; Low and Reed,2000; Rennie,1998; Taylor et
al,1987) although they require verification.
CLAIMED ANALGESIC MECHANISMS
AND SUGGESTED AMF’S
THEORETICAL ANALGESIC
MECHANISM
SUGGESTED AMF (AUTHOR)
‘PAIN GATE’/SENSORY FIBRE
STIMULATION
1-100Hz (WADSWORTH AND CHANMUGAM,1980)
80-100Hz ( DE DOMENICO,1982), 90-100 Hz (SAVAGE,1984)
100Hz (GOATS,1990)
INCREASED CIRCULATION/
SYMAPTHETIC FIBRE
STIMULATION
0-100Hz (WILLIE,1969); 0-5Hz (SAVAGE,1984)
100 Hz (GANNE,1976, NIKOLOVA,1987); 100Hz, 90-100Hz, 1-100Hz
(WADSWORTH AND CHANMUGAM,1980) ; >80Hz (DE DOMINICO-
1982)
DESCENDING PAIN
SUPRESSION/ NOCICEPTIVE
FIBRE STIMULATION
10-25Hz (DE DOMINICO,1982) ; 130Hz (SAVAGE, 1984);
15Hz (GOATS-1990)
PHYSIOLOGICAL BLOCK OF
NOCICEPTIVE FIBRES
PLACEBO RESPONSE
C FIBERS>50Hz; Aδ FIBERS>40Hz (DE DOMENICO,1982); 40Hz LARGE
DIAMETER/<40Hz SMALL DIAMETER (GOATS, 1990)
NONE SPECIFICALLY IMPLICATED
THERAPUTIC EFFECTS
 Using high AMF (70-150 Hz) for acute problems and pain, and frequencies below 50Hz
for chronic and sub-acute conditions and where muscle contraction is required.
 A placebo effect, which occurs in all treatments, is likely, especially since interferential
machines are technically impressive and produce a distinct, somewhat unusual but not
unpleasant sensation.
 Muscle contraction can also be achieved at higher current amplitude without any
significantly uncomfortable skin sensation.
 Stress incontinence in females (Laycock and Green, 1988), males (Laycock and Jerwood,
1993) using the bipolar technique increased strength in the pelvic floor muscles.
INDICATIONS
 Pain relief/ anesthetic effect by stimulating the release of endorphins and
blocking the transmission of pain impulses (pain gate mechanism)
 Increase in blood flow to promote tissue healing and reduce
swelling/inflammation
 Muscle stimulation to activate weak muscles and overcome muscle
inhibition caused by the injury.
CONTRAINDICATIONS
 Patients with cardiac pacemakers.
 Near the low back or abdomen of pregnant women
 Local malignancy
 Loss of sensation
 Strong muscle contraction might cause joint or muscle damage, detachment of a
thrombus, spread of infection, and haemorrhage.
 Stimulation of autonomic nerves might cause altered cardiac rhythm or other autonomic
effects.
 Currents might provoke undesirable metabolic activity in neoplasms or in healed
tuberculous infections.
REFERENCES
 Physiological effects of IFT, Electrotherapy evidence based practice by
Sheila Kitchen.
 Interferential Current, Electrotherapy explained , John Low and Ann Reed.
 Electrotherapy.org
THANK YOU!

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Interferential therapy

  • 1. PHYSIOLOGICAL EFFECTS OF IFT BY: DR. LAKSHMI PAVANI P. (PT)
  • 2. INTERFERENTIAL CURRENT  Is essentially a medium-frequency current (normally approximately 4000 Hz)  Rhythmically increases and decreases in amplitude at low frequency (adjustable between 0 & 200-250 Hz)  Produced by mixing two low frequency currents that are slightly out of phase, either by applying them so that they ‘interfere’ within the tissues , or alternatively by mixing them within the stimulator prior to application (pre-modulated current)
  • 3. PHYSIOLOGICAL EFFECTS OF IFT Analgesic effects :  The ‘pain-gate’ theory.  Descending pain suppression  Physiological block of nerve conduction  placebo
  • 4. Other effects:  Muscle stimulation  Increased blood circulation  Edema reduction  Placebo
  • 6. NOCICEPTORS  Sensory receptors located at free endings of Aδ and C fibers  Detect noxious stimuli  Carried to the CNS  Found in skin, viscera, muscles, joints, and meninges  They are stimulated by the inflammatory mediators released by the damaged tissue eg: bradykinins
  • 7. SKIN NOCICEPTOR TYPE OF STIMULI Aδ MECHANOSENSITIVE MECHANICAL Aδ MECHANOTHERMAL THERMAL C POLYMODAL MECHANICAL, THERMAL, CHEMICAL
  • 8.
  • 9. PRIMARY AFFRENT FIBERS  Nerves that carry input from the periphery to the spinal cord.  3 types: Aβ, Aδ and C fibers FIBRE TYPE STIMULI ACTIVATION THRESHOLD DIAMETER MYELINATION TRANSMISSIO -N Aβ NON-NOXIOUS LOW LARGEST HIGH RAPID Aδ NOXIOUS, RAPID, SHARP, LOCALISED PAIN HIGH AND LOW SMALL MODERATE QUICK (but not as fast as Aβ) C NOXIOUS, SLOW, DULL, NON- LOCALISED PAIN HIGH SMALLEST LOW VERY SLOW
  • 10. TRANSMISSION IN THE DORSAL HORN  Dorsal horn a.k.a Posterior column  Grey matter within the posterior horns of spinal cord  Primary afferent nerves release the excitatory neuro-transmittors  Secondary afferent neurons synapse with Aδ and C fibers  Activity of secondary neurons is affected by the activity of the afferent neurons, interneuron and efferent neuron pathways.
  • 11.
  • 12. ASCENDING THE SPINAL CORD  2 main pathways carry nociceptive signals up the spinal cord to the brain. a) spinothalamic tracts b) spinoreticular tracts  Pain processing in the brain a) thalamus b) primary and secondary somatosensory cortex c) prefrontal cortex
  • 13.
  • 14. INHIBITING THE PAIN TRANSMISSION 1) GATE CONTROL THEORY 2) DESCENDING INHIBITORY PATHWAYS 3) PHYSIOLOGICAL BLOCK OF NERVE CONDUCTION
  • 15. 1) GATE CONTROL THEORY  Melzack and wall -1965  Inhibition at spinal cord level / pre synaptic inhibition Eg: Rubbing your head after bumping it Activates Aβ fibers Activates inhibitory interneurons Inhibits pain transmission by C fibers
  • 16.
  • 17.  Transmission cell- ‘T’ in dorsal horn which prefers mechanoreceptor information rather than nociceptor information.  Nociceptive fibers i.e Aδ and C fibers relay in the more superficial lamina i.e say lamina 1 of the dorsal horn + areas of substantia gelatinosa.
  • 18. IMPULSES FIRE ON THE POLYSYNAPTIC INTERNEURONS PROGRESS TO THE HIGHER CENTERS BY THE SPINOTHALAMIC TRACT TO THE THALAMUS AND THEN THE PARIETAL LOBE
  • 19. POLYSYNAPTIC INTERNEURONS  They are cell bodies with dendrites present in the grey matter of the spinal cord. (present in the dorsal horn too)  Responsible for evoking motor response Eg: when we suddenly step on a thorn Sensory response- knowing that there was pain, location of the pain Autonomic response- HR, RR
  • 20.  Mechanoreceptors – rely on the polysynaptic interneurons in the deeper lamina of the dorsal horn and synapse with the spinocerebellar tract/ dorsal columns.  When there is increase in the mechanoreceptor activity, signals from the polysynaptic interneurons are not only transmitted to the spinothalamaic tract and dorsal column, but also fire back into the areas of Lamina 1 where the nociceptors usually fire.  Leading to a block in the polysynaptic interneurons in the nociceptor Lamina no pain conduction pre synaptic inhibition.
  • 21. 2) DESCENDING INHIBITORY PATHWAYS  Electrical stimulation of the periaqueductal grey matter (PAG) area can produce analgesia, demonstrated through electrophysiological and pharmacological studies that ‘descending influences’ on spinal nociceptive processing involves the PAG and the Rostral Ventromedial Medulla (RVM) (Fields, Milan -1960)
  • 22. (Dorsal root ganglion Periaqueductal grey matter Rostral ventromedial medulla (Dorsal horn) (Nucleus Raphe magnus)
  • 23. Incoming painful stimuli are transmitted to the dorsal horn to the raphe nuclei, especially the nucleus raphe magnus, in the upper medulla to the periaqueductal grey (PAG). Descending impulses pass back Rostral ventromedial medulla (RVM) to the dorsal horn via reticulospinal fibers.
  • 24.  The periaqueductal grey matter (PAG) and the rostral ventromedial medulla (RVM) contain high levels of opioid receptors  Inhibition of the pain pathway occurs monoaminergically, releasing inhibitory neurotransmitters at the spinal level. (Goats 1990, Rennie 1988)  i.e through mono amine nerve transmitters – Nor adrenaline, dopamine, serotonin – also known as catecholamines.  Resulting analgesia may be long lasting , but pain may initially increase owing to the stimulation of nociceptive Aδ and C fibers (Goats,1990)  Post synaptic inhibition/ descending pain inhibition.
  • 25. 3) PHYSIOLOGICAL BLOCK OF NERVE CONDUCTION  Stimulation of peripheral nociceptive fibers at rates above their maximum conduction frequency may cause cessation of action potential propagation (De Domenico, 1982; Goats,1990; Low and Reed,2000; Rennie 1988; Shafshak, El-Sheshai and Soltan, 1997), caused by increased stimulation threshold and synaptic fatigue (Goats,1990)
  • 26. OTHER EFFECTS 1) MUSCLE STIMULATION:  Stimulation of the motor nerves can be achieved with a wide range of frequencies. Clearly, stimulation at low frequency (e.g. 1Hz) will result in a series of twitches, whist stimulation at 50Hz will result in a tetanic contraction. (Low And Reed; shafshak,El-Shehai and Soltan,1991)
  • 27. 2) INCREASED CIRCULATION & EDEMA REDUCTION  Interferential current has been claimed to improve the circulation of blood and swelling, which may wash away the chemicals that stimulate nociceptive nerve endings (De Domenico, 1982; Goats,1990; Rennie 1988; Shafshak, El-Sheshai and Soltan, 1991)  Reduced swelling may concomitantly reduce tissue pressure. These phenomena are reported to occur because of mild muscle contraction or action on the autonomic nervous system, decreasing the tone of blood vessels ( Low and Reed; Shafshak,El- Sheshai and Soltan,1991)
  • 28. 3) PLACEBO:  Placebo responses have been identified in the literature as a potential factor with IC stimulation (De Domenico,1982;Goats,1990; Low and Reed,2000; Rennie,1998; Taylor et al,1987) although they require verification.
  • 29. CLAIMED ANALGESIC MECHANISMS AND SUGGESTED AMF’S THEORETICAL ANALGESIC MECHANISM SUGGESTED AMF (AUTHOR) ‘PAIN GATE’/SENSORY FIBRE STIMULATION 1-100Hz (WADSWORTH AND CHANMUGAM,1980) 80-100Hz ( DE DOMENICO,1982), 90-100 Hz (SAVAGE,1984) 100Hz (GOATS,1990) INCREASED CIRCULATION/ SYMAPTHETIC FIBRE STIMULATION 0-100Hz (WILLIE,1969); 0-5Hz (SAVAGE,1984) 100 Hz (GANNE,1976, NIKOLOVA,1987); 100Hz, 90-100Hz, 1-100Hz (WADSWORTH AND CHANMUGAM,1980) ; >80Hz (DE DOMINICO- 1982) DESCENDING PAIN SUPRESSION/ NOCICEPTIVE FIBRE STIMULATION 10-25Hz (DE DOMINICO,1982) ; 130Hz (SAVAGE, 1984); 15Hz (GOATS-1990) PHYSIOLOGICAL BLOCK OF NOCICEPTIVE FIBRES PLACEBO RESPONSE C FIBERS>50Hz; Aδ FIBERS>40Hz (DE DOMENICO,1982); 40Hz LARGE DIAMETER/<40Hz SMALL DIAMETER (GOATS, 1990) NONE SPECIFICALLY IMPLICATED
  • 30. THERAPUTIC EFFECTS  Using high AMF (70-150 Hz) for acute problems and pain, and frequencies below 50Hz for chronic and sub-acute conditions and where muscle contraction is required.  A placebo effect, which occurs in all treatments, is likely, especially since interferential machines are technically impressive and produce a distinct, somewhat unusual but not unpleasant sensation.  Muscle contraction can also be achieved at higher current amplitude without any significantly uncomfortable skin sensation.  Stress incontinence in females (Laycock and Green, 1988), males (Laycock and Jerwood, 1993) using the bipolar technique increased strength in the pelvic floor muscles.
  • 31. INDICATIONS  Pain relief/ anesthetic effect by stimulating the release of endorphins and blocking the transmission of pain impulses (pain gate mechanism)  Increase in blood flow to promote tissue healing and reduce swelling/inflammation  Muscle stimulation to activate weak muscles and overcome muscle inhibition caused by the injury.
  • 32. CONTRAINDICATIONS  Patients with cardiac pacemakers.  Near the low back or abdomen of pregnant women  Local malignancy  Loss of sensation  Strong muscle contraction might cause joint or muscle damage, detachment of a thrombus, spread of infection, and haemorrhage.  Stimulation of autonomic nerves might cause altered cardiac rhythm or other autonomic effects.  Currents might provoke undesirable metabolic activity in neoplasms or in healed tuberculous infections.
  • 33. REFERENCES  Physiological effects of IFT, Electrotherapy evidence based practice by Sheila Kitchen.  Interferential Current, Electrotherapy explained , John Low and Ann Reed.  Electrotherapy.org