IFC and Tens Flashcards
General Overview of IFC and TENS
TENS and IFC use electric currents to stimulate peripheral nerves resulting in short-term pain relief (minutes to hours)
What is pain?
Unpleasant sensory and emotional experience associated with actual or potential tissue damage (acute-new to 3 months, persistent, chronic – synonymous with persistent)
Nociceptive input neither sufficient nor required
Ex: Nail in head vs paper cut
PERCEPTION
What is the biggest nerve type?
A Alpha Fibers
Ia afferent (Aa)
Myelinated: Yes
Conduction Velocity: 70-120 m/s
Specialized Ending: Muscle Spindle
Receptor Location: Skeletal Muscle
Sensory Function: Joint position/Movement
1b afferent (Aa)
Myelinated: Yes
Conduction Velocity: 70-120 m/s
Specialized Ending: GTO
Receptor Location: Musculotendinous junction
Sensory Function: Muscle Contraction Force
II afferent (AB)
Myelinated: Yes
Conduction Velocity: 25-70 m/s
Specialized Ending: Touch Receptors, Joint Receptors, Muscle Spindle Secondary
Receptor Location: Skin, Joint Capsule, Skeletal Muscle
Sensory Function: Touch/Pressure, Joint position/movement, Joint Position
What are the areas of the body process pain?
Dorsal Horn in Spine and Brain
- Each location can cause for the signal to turn up or turn down
- Brain is the only thing that can indicate pain.
Two mechanisms of pain inhibition we use clinically
Gate theory control (local spinal cord level)
Descending Pain Control (both supraspinal and spinal level – can be more systemic)
- Indigenous Opioids
- Internal NTs
Pain Gate Theory
Two sub-mechanisms:
- Basic mechanism: Highway analogy – explains temperature effects on pain perception: more temp sense = less “pain” sense
- Synaptic inhibition - explains effects of touch on pain (puscinian corpuscle, etc.)
Pain Gate Theory - Highway Analogy
- Temperature effects on pain perception: more temp sense = less “pain” sense
- Sensation and Nociception both carry Delta A and C (Travel into **spinal cord **at dorsal root ganglion at synapse)
Pain Gate Theory - Synaptic inhibition
- Stimulation of other receptors causes transmission on AB axons
- At spinal level, AB axons excite an interneuron which then inhibits the transmission of nociception in the spinothalamic tract (with the Delta A and C fibers)
- There are various types of inhibition and neurochemicals involved (pre- and post-synapse, GABA and Enkephalin, and probably others)
- Pain system is complex
Pain Gate Theory occurs….
locally at the levels of the spinal cord involved with peripheral stimuli
Descending Pain Control
(Endogenous Opiate System)
Two systems operate at supraspinal level to impact:
1. Involved spinal cord level through neural connections from the periaqueductal gray (PAG) and Raphe Nucleus
2. General Systemic Effects
Involved spinal cord level through neural connections from the periaqueductal gray (PAG) and Raphe Nucleus
(Both in midbrain and have direct connections in spinal cord; in the spinal cord where it ends releases release enkephalins, norepinephrine, serotonin – inhibition effects)
Ex: Stub toe, this system kicks in to dull pain. Kick in a minute or two after initial stub of toe.
General Systemic Effects - Descending Pain Control
Hypothalamus and Pituitary
1. Beta Endorphin and Dynorphin (Dumped in blood)
a. Widespread release through CNS and circulatory system – explains the classic exercise pain inhibition or “runner’s high”
b. One of the best ways to stimulate this is through exercise
Endogenous Opiate System
Works locally and systemically
These mechanisms work together and simultaneously, HOWEVER, it is convenient to conceptualize them as being recruited progressively as the pain experience intensifies or persists
Longer half life
Other mechanisms involved in pain modulation – Placebo Response
Symptom improvement based on expectation, a possibility with any intervention
For E-stim, reported as high as 30-40% of the response
Response can be blocked by Naloxone, and opiate anatagonist meaning placebo is a neurophysiologic response!
Other mechanisms of pain modulation with E-stim Vasodilation
Areas of myofascial pain (trigger points) may be ischemic, contributing to pain experience
Electrical stimulation induces local vasodilation in patients with myofascial symptoms
Vasodilation may reduce ischemic pain
Indications for TENS (sensory component)
Treating pain syndromes
- Acute
- Chronic
- Post-Op
- Neurological (Ex: Shingles)
- Phantom
Before/during painful treatments
- Stretching
- Debridement
Indications – Populations with Evidence of TENS efficacy
LBP
Neck pain
Myofascial pain
RA
OA
Dysmenorrhea
Labor/post labor
Post op pain: abdominal, thoracic, shoulder
Painful shoulder post CVA (stoke)
Peripheral neuropathy
Trigeminal neuralgia
Headache (migraine and other)
Post amputation and phantom limb
Acute pos-traumatic
And others…
Precautions for TENS
Cardiac pacemaker
- Recommend ECG monitoring for 1st treatment
Implantable Cardioverter defibrillator
- Need to inactive during sessions
- ECG monitoring
Allergic skin reactions under electrode
Low cognitive function
Monitor Caffeine intake (3 cups/day or 200 mg/day; Can reduce effect)
Abnormal skin sensation
While driving
Keep out of reach of children
Be aware of medication usage (Ex: Opiods)
Neural Depolarization
When considering activation of neural tissue with current, you must consider
- Relative size and myelination of neurons
– Larger are easier to stimulate
- Anatomical depth of tissue relative to depth of penetration of current
–Closer to the surface are easier to stimulate
Typical Equipment - TENS/IFC
Intensity/Amplitude
Pulse rate/Frequency
Pulse duration
Common Wave characteristics:
- Biphasic with a negative spike component
- Monophasic with a positive rectangular component only (Charge imbalance, may get skin irritation)
Some modulation (change) option
Typical Tens Devices
Battery Operated
Common ranges on parameters:
Pulse duration range
20-200 usec
Pulse rate (frequency) range
1-150 pps
Amplitude (intensity) for each channel range
1-80 mA
