Electricity

- Intro to electricity
- Soft tissue healing + Biofeedback
- Pain
- Muscle contraction
Laser
Special topics

Electricity
- Intro to electricity
Electrical current = flow of charged particles
History = mm contractions in frogs, motor points, law of excitation, intensity and
duration of stimulus

Waveforms
Waveform = current in a graphic representation of the current flow over time
Vertical axis = direction of current flow + or –
Horizontal axis = time
Types of Waveforms:
1. Direct current
a. Continuous stream of charged particles flowing in ONE direction
b. Electron flow longer than 1 sec.
c. SINGLE ploarity (monophasic)
d. Leaves a residual charge in tissue
i. Iontophoresis
ii. Stimulating DENERVATED muscle
2. Alternating current
a. Continuous, wavey (sinusoidal) BIPHASIC -/+ flow of charged particles
b. EQUAL ion flow in each direction (NO charge left in tissue
i. Pain control = IFC interferential current
1. Premodulated current
ii. Muscle contraction
1. Russian
3. Pulsed current
a. Interrupted flow of charged particles where the current flow is in series of
PULSES separated by periods of no current flow
b. MONOphasic or BIPHASIC
c. Equal ion flow in each direction (NO charge left in tissue)
i. Monophasic = tissue healing + acute edema
1. High-Voltage pulsed current (HVPC)
ii. Biphasic = Most common = pain control + mm contraction
1. Symetrical – speed and total amount of current flow are the SAME
in both phases (nice for LARGER mm groups)
2. Asymetrical – spped of current flow is DIFFERENT in each phase
 a. Balanced = total amount of current is SAME (good smaller
mm group / kids)
b. Unbalances = total amount of current is DIFFERENT =
charges left in tissue

Ionic Effects of Electrical current

 Electrical charge = quantity of unbalanced electricity in body
 Most = biphasic waveform and leave NO charge in tissue
 DC, pulsed monophasic, and unbalanced biphasic DO LEAVE A NET CHARGE
 Negative electrode (cathode)
o Attracts + charged ions and repels - ions
 Positive electrode (anode)
o Attracts – chraged ions and repels + ions
 THERAPY helps with iontophoresis (pushing meds), inflammation, tissue healing, reduce
edema
Parameters Definition
DC: current flows equally throughout the stimulation time
Amplitued = AMOUNT of current flow
Time
AC and PC: current flow varies over time
Amplitued = AMOUNT of current flow
 Magnitude (strength/intensity)
 Measures higher # = higher amp. / volts
o Ramp up = time it takes for current amplitued to INCREASE from zero to max
o Down = time for current amp to DECREASE to zero
o = improve comfort
Time
Duration = how LONG current flows
 Phase = perod when current flows in ONE direction
 Phase duration = length of phase
 Pulse = period when current flows in ANY direction
 Pulse duration = length of each puls
 Interpulse interval = time between PULSES
Frequency = how OFTEN current flows
 # of cycles / sec = AC
 Freq. Inverse with cycles
 # of pulses / sec = PC

Mechanisms to stimulate action potentials in nerves

Electricity and Nerves:
 Electricity = DEPOLARIZING nerve membranes = Produce Action potentials
o Resting membrane potential: Inside cell is NEGATIVE / outside is POSITIVE
  Maintained with more Na+ ions on outside of cell and fewer K+
ions inside
o Depolarization
 With enough STIMULUS, NA channels open and rush into cell = MAKE
inside POSITIVE
 @ +30 mV K+ channels open and rush out of cell
o Action potential = All or None : Reached at a threshold
 Amount of electricity required to produce a AP based on NERVE TYPE
 Strength-duration curve
o AP propagation
o Physiological stimulation (contracting you muscle your self) = AP travels in ONE
direction
o Electrical stimulation – AP travels in BOTH directions (distal & proximal)
o Speed
 Larger diameter of nerve = FAST AP
 Myelinated nerves = FASTER

 Sensory nerves = low current/ short duration

o 50 – 100us
 Motor nerves = high current; long duration
o Muscle 150-350 us
o Smaller muscel 100-125us
 Below 1 ms will help to minimize pain (AVOID C fibers)

+ clinical effects of electrical currents

Contras and precautions

Contraindications for Electricity
 Hypersensitivity to electricity
 Over carotid sinus
 o May induce rapid fal lin BP and HR = faint
 Over arterial/ venous thrombosis or thrombophlebitis
 Pregnancy
 Unstable arrhythmias, cardiac defibrillator
 Pacemaker – demand

Precautions
 Cardiac disease
 Imparied Mentation or sensation
 Malignant tumors
 Skin irritation or open wounds

Adverse effects:
 Burns, skin irritation , painful

Electrode placed:
 Smooth over skin
 Not over superficial bone
 Current Deeper when further apart
 Size of electrode dictates current density at pads

Applications in Rehab
- Pain
o How to chooce electrotherapy:
Treatment purpose
ID neurophysiologic response needed:
Sensory, motor, noxious
How to manipulate parameters to effect neurophys response (type / magnitude
Choose appropriate device

o Pain pathways and modulation of pain

Nociception = NEURAL process of encoding noxious stimuli
 Transmission can be facilitated or inhibited at several points in system BEFORE conscious
perception
o Nocioceptors = Free nerve endings
 Active via mechanical, thermal, chemical stimuli
 Produce AP to triger stimulus
o Nociceptive signals = transmitted to CNS by PRIMARY AFFERENT neurons with dif
functions
 C-fibers and A-delta = nociceptive
 A-beta fibers transmit NON-nociceptive input
Fiber Type of signal Size, myelination? Pain type Blocked by gate or
opioid mech?

A-Delta Sharp, stabbing, or pricking Small, thin Acute pain Not blocked by
pain Localized opiods
Quick onset, short lasting Not emotional
C Fibers Dull, throbbing, aching or Smaller than ^^ , Chronic pain Reduced by
burning non-myelinated Diffuse localize opioids
Slow onset, long lasting emotional
A-beta Non-nociceptive Larger, Myelinated N/A Role in Gate
Vibrations, stretch skin, Fast conduction control
mechanoreception mechanism

Pain= unpleasant sensory and emotional experience associated with actual or potential tissue
damage
 OUTPUT of brain triggered part of the process by which afferent AP are converted into
conscious awareness
 Pain experience = 3 dimensions
1. Sensory-discriminative – where pain is felt and what it feels like
2. Motivational-affective- how pt feels EMOTIONALLY about it
3. Cognitive-evaluative – what pt thinks abouth the pain and what they expect result
from pain is
 pain not always reliable indicator of state of tissues

o Mechanisms of pain modulation with electricity

Modulation of Nociception in brain
 Cognitive, emotional, and social anc contextual factors MODIFY input
 Unconscious evaluation of degree of threat = MOST important factor of pain matrix
 Brain EVOLVES with interpreting nociception + making pain experience over time
o Chronic pain = more active prefrontal cortex = more emotional links vs acute
 Electrically stim AP in SENSORY and motor nerves = control pain
o Gate Control
o Opioid release

Gate Control – High-frequency TENS = stims A-beta nerves

 @ substantia gelatinosa @ spinal cord level
o A-beta fibers = INHIBITORY INPUT = PRE-synaptic inhibition
 CLOSES the gate to the transmission of noxious stimuli from SPINAL CORD
to brain
o A-delta/ Cfibers = excitatory input = more noxious stim thru

Endogenous Opioid System of Pain Modulation

  Opiopeptins = opiod-like peptides (endorphins)
o Indirectly INHIBIT nociceptive transmission by INHIBITTING release of GABA in
PAGM + raphe nucleus
 GABA inhibitis activity of pain-controling structures (a-beta) PAGM Raphe
nucleus) and can INCREASE nocicptive transmission to Spinal cord
 Control pain by BINDING to specific opioid receptors
 @ many PERIPHERAL NERVE ENDINGS and in neurons in NS
o Periaqueductal gray matter PAGM and raphe nucleus of brainstem
 Induce analgesia when electrically stimmed.
- Location:
o Superficial layers of dorsal horn of spinal cord
o Limbic system
o Enteric NS
o Nerve endings of C fibers
 Opioids / opiopeptins = PRE-synaptic & POST-synaptic inhibition
 E-stim controls pain by stimulating the production of endorphins and enkephalins
(endogenous opioids)
o Act similar to morphine = modulate pain perception by BINDING TO opiate
receptors in BRAIN and other areas = act as NT
o Opioids also activate DECENDING inhibitory pathway that invole
 Low-rate TENS = longer lasting (4-5hours of pain control)
o Can develop tolerance with it ^^ so NEED frequency modulations so body no
adapt
 Electroacupuncture and acupuncture-like TENS
o Opiod sys mechanism explains pain-releiving effects of painful stim as bearable
levels of pain stim = causes sensation of burning = reduce intensity of less
bearable preexisting pain in area of application. Adding a nice ouch to the bigger
ouch to forget the bigger one
o Electroacupunture
 Evidence: reduce pain, stiff, diability with OA of knee
 Post-op pain reduced in frozen shoulder
 RA
 Decrease post-op pain effectiveness vs high-rate TENS
o Acupuncture-like TENS
 INCREASE intensity to produce painful noxious stim = thru A-delta nerves
 Endogenous opioid mech
 Evidence: decrease chronic neck pain w/ exercise + decrease post-op pain
and analgesic after spinal surgery

Story: GABA = Inc ascenting pain transmission = going to tell brain about ouchie
Opiopeptins STOP Gaba release so donʻt tell brain

o Evidence for electrical current for pain control and INDICATIONS

 o Modulation and accommodation

TENS- trancutaneous electrical nerve stimulation

Modulated = varies over time to decrease adaption = decrease in frequency of AP and a
drcease in subjects sensation of a stimulus when applied
With Modulation can change 3 parameters all with equal effects = prevent adaption
Intensity can turn up (amplitude)
Change frequency
Change pulse duration
Indivations: + evidence
 Post-stroke to reduce post-stroke spasticity
 Wound care in older adults with pressure injurry = reduce pain + improve tisssue healing
rates
 meh (low evidence) for neuropathic pain

o Applications of electical current for pain control

TENS
IFC – interferential current
o 2 alternating current with different frequencies
 In Phase = combine INCREASE amplidude
 Out phase = combine to DECREASE amplitude
o Therapeutic BEAT frequency = 100 Hz
o Cannot select pulse duration – MUST cross channels
o Stim larger areas, more comfortable vs TENS, decrease or control inflammation
or ischemia
COMBO – US with Estim
Electrode placement:
o Around painful area, trigger points
o If cannot go by pain = PLACE IT PROXIMMALLY to pain site along sensory nerves
supplying the area

- Muscle contraction
Different types of e-stim for contraction
 NMES – Neuormuscular Electrical stimmulation = innervated mm.
o Stimulates AP along motor nerves
o Broad application: orthopedic donditions, pt with neurologic injury (stroke, sci),
to manage edema (mm pump)
 EMS – Electrical muscle stimulation = Denervated mm
o Stims AP in muscle cell directly (without input from motor nerve
o DC or PC >10ms or longer
Physioloically initiated mm contraction and electrically stimulated mm contractions
Physiologically initiated Electrically stimulated
 Smaller nerve fibers = SLOW-TWITCH  Largest diameter nerve fibers
type 1 mm fibers  = FAST TWITCH type 2 mm fibers
o Produce lower force o Produce stronger and quicker
o More resistant to fatigue and contractions
atrophy o Fatigue more rapidly and more
 Gradual increas in force smoothy prone to weakening and
graded atropy with disuse
 Rapid, and JERKY onset
 Stims ALL motor untis at same time
when reach threshold
Best when combined
Physiological contractions with estim contractions to optimize the recruitment of all muscle
fibers and functional integration of strength gains

Clinical applications of electrical stimulatio for mm contraction and evidence

NMES continued...
Used for
 Strengthening muscle
o Mechanisms: Overload principle = greater the load applied to a muscle, the
stronger it must contract and then the more strength it will gain
 Physiological – load progressively increased by increase resistance
 Electrical current = increase FORCE by increase total amount of CURRENT
 Inc pulse duration, amplitude, electrode size
 + external resistance
o Specificity principle = muscle contractions specifically strengthine the muscle
fibers that contract
 Stim = more effect on type 2
 After surgery or imobilization, e-stim amplify and accelerate strength
gains
o Evidence for strengthening:
 Post ACL reconstruction: quadriceps strengthening key = NMES + exercise
greater strength gain
 Post- total knee arthroplasty (TKA): quad strngth key – aging may lead to
type 2 fiber atrophy
 NMES + exercise following surgery improves quads
 NMES beofre surgery = greater post-op strength and rapid
functional gains
 Non-surgical management of knee conditions
 OA -decrease pain, improve quad strengthm inprove function
  RA – improve muscle strength and endurance
 Increase UE strength after immob.
 COMBINED with exercise; may NOT lead to improved functional
performance
 Imporve endurance
o Evidence for Cardiac, pulmonary or critical illness
 STRONG – NMES is effective for improving mm strength and functional
outcomes in wide variety of critical illnesses
 Heart failures: NMES to quads = improved peak O2 uptake, 6 min walk
test distance (endurance), muscle strength, depressive symptoms, and
QOL
 Critically ill pts: NMES + rehab increased or better perserved mm
strength and muscle mass vs control standard
 Prevent or slow atrophy
 Reduce spasticity
 Help restore motor function
o Neurological conditions: Post-stroke
 NMES can increase strength, reduce spacsticity, and enhance functional
recovery after stroke
 Reduce shoulder subluzation if applied early following stroke
 Enhance descending control of mm activity and coordination
 Provide cue to pt. To activate a mm group
 reduce spacsticity By stimulating antagonist contraction (reciprocal
inhibition)
o Functional electrical stimulation FES
 Electrial stim of mm contractions to perform functional activities
 Stim. DF via nerve during Swing phase of gait
 Ankle-foot orthosis AFO subsitute
o Spinal cord injury
 **does NOT reverse SCI
 May reduce disability
 Produce movements for exercise FES
 LMN and neuromuscular junctions must be intact
 NOT painful
 Produce sufficient enough contaction to carry out activity
o TBI, MS, CP (need intact peripheral nn. System)
o Pelvic Floor: urinary incontinence , overactive bladder

o Edema Control
 Using MONOPHASIC, sensory level stim for INFLAMMATION EDEMA
 Use mm contraction estim for POOR PERIPHERAL CIRCULATION DUE TO
LACK OF MOTION EDEMA
  Combined with elevation of extremeity.
 Reduce risk of DVT
o Evidence: NMES to calf mm found to be 1.7 to 3x more
effective than intermittent pneumatic compression for
promotine venous circulation
 EMS – Electrical muscle stimulation = Denervated mm
Motor denervation  paralysis, mm atrophy  fibrosis
o Onging e-stim may STOP or reverse loos of strength, atrophy fibrosis
o After stimulation, improvments may stop persisting
o USE DC or PC with pulse duration of 10 ms or longer = EMS
o Bell palsy pt
Parameters and considerations for application
Tables in slides
Electrode placement NMES:
 1 Over the motor point for muscle
o = place where e-stim will produce the greatest contaction with least amount of
electricty
 Where motor n enter mm. (middle of mm belly)
 Other over muscle to be stimulated = PARALLEL to direction of mm fibers
 At least 2 inches apart (1in when mm contracted)

NMES waveform = Pulsed biphasic

Russian = AC @ 2500Hz

Pulse Duration = 125- 350 us to stim AP in motor nerves

 Shorter = more comfy for smaller muscles ( but need HIGHER amplitude of current to
achieve the same strength of muscle contraction)

Frequency:
< 20 pps small mm 30 pps large mm
seperate twitches = small mm or children
35-50 pps twitche slose together, smooth tentanic contraction
50-80 pps stronger contraction but more rapid fatigue

On-Off time: limits fatigue

Strengthening: 1:5 ratio (6-10 ON / 50-120 off)
Reduce muscle spasm and edema pump 1:1 (2-5 sec)

Ramp time
o Gait training = NO use
o Spasticity reduction via contraction of antagonist to spastic mm = longer ramp
time to avoid rapid stretch of agonist
MVIC – maximum voluntary isometric contraction
 Strengthenign : injured >10% of the MVIC of uninjured limb (see contraction)
o Without injury > 50% see joint movement
 Mm re-edu: use lowest current needed to get outcome
 Reduce mm spasm or edema = only need visible contraction

- Soft tissue healing + Biofeedback

Wound Healing PT:
 Diabetes: foot ulcers and infection bc of peripheral vascular disease
 Spinal Cord Injury: untreased pressure ulcers
Wound Care:
 Interprofessional = PT = tissue healing for SOFT tissue
 E-stim = adjunct to other wound care things
CURRENT TYPES:
 Direct application of current to wound
 Indirect = control edema , deliever meds

Waveforms: Needs to leave an ionic effect

Monophasic
DC
HVPC = PC
Mechanism for electrical + tissue healing
GALVANOTAXIS:
 Directional movment of cells in response to an electrical field
 Injured tissue: ruptures cell membranes, charged ions LEAK out of cells = center of
wound becomes electricaly charged relative to surrounding tissue
o Skin battery = electrical current that ACTIVATES HEALING
o ^^^^ this can be increased with e-stim
 Galvanotaxis = cause specific cells (neutrophils, macrophages, lymphocytes, fibroblast to
MOVE to an injured healing area bc these cells carry a charge
o Phases of tissue healing matter:
o Negaive electrode – treat infected or inflamed wounds
o Positive electrode – if necrosis without inflammation present AND when would
is in proliferative stage of healing
 E-stim attracts cells to an injury site AND ACTIVATES them!!!!
o Fibroblasts = proliferative stage = e-stim enhances their REPLICATION and
synthesis of DNA
o Peak voltage 60-90 V
 Monophasic PC = Galvanotaxis only happens with NET CHARGE

Antimicrobial Effects:
 E-stim may promote healing via antimicrobial activity
 Monophasic DC or HVPC shown to KILL bacteria
 o Current needs to be at HIGHER voltage or for LONGER that feasible in clinic to
inhibit growth
o = UNLIKELY MECHANISM
 May enhance activity of anitbiotic agents against bacteria in biofilms

Enhanced Ciruclation:
 E-stim may facilitate tissue healing by increasing circulation
o Due to acceleration of angiogenesis

 NOT as effective as warm room

Application + evidence
Parameters

Define biofeedback + describe it in rehab

Proposed physiologica effects of EMG biofeedback
Clinical applications + evidence

Iontophoresis = DC
Benefit: deliever therapeutic drug while avoid side effects
Mechanism: like charges repel
A fixed electric charge can PUSH chreged ions of drug through skin

40mA-min

Dexamethason (anti-imflammaroty) negative charge = ELECTODE = NEGATIVE on drug pad

=SAME polarity

Check skin

Biofeedback:
Provides information to user about their own physiological or biomechanical process to IMPOVE
self-awareness and control

Direct = heart rate monitor (INTERNAL biological)

INDIRECT = TRANSFORMED = external procced info
- Not percise EMG biofeedback
- NO a direct a measure of mm contraction
- DOES NOT PRODUCE ELECTRICITY

LIMIT noise =
Clean skin, orient electrodes paralle, secure
  Excitation (facilitate)
 Inhibition – sown training
 Coordination

STRONG EVIDENCE for pelvic floor

Gain setting (C) : the higer the gain (amplificatio) the higer the SENSITIVITY of an EMG
SENTIVIE

LASER:
Thermal : increase tissue temp
Nonthermao – no temp inc. UV, Low levels of pulsed diathermy, LIGHT

 Light = eneryg visible or near visible

 Laser light therapy = PHOTOBIOMODULATION Therapy PBM

LASER = light amplification by stimulated emission of radiation

 Monochromatic + coherent (inphase)

Common form = 3B <500 mW low level therapy = can CAUSE permanent eye injury with brief
exposure + burns

Wavelength = LONGER THE WAVE = greater the depth

Deep to superficial effect: Laser > SLD > LED

When power and wavelength are the same

POWER = 5-500mW
ENERGY = J (Joules) = P x time
HIGHER THE POWER = the SHORTER the time

ENERGY DENSITY = J/cm2

Mechanism of Action: absorption of the light energy by the CHROMOPHORES increase the
oxidative metabolism in mitochondria
- INCREASE ATP

Arndt-Schultz Law: Too little power = no effect

Too musch = HURT
Minimum stimulus needed to initial biological process
Effects of laser:
ATP = STRONGEST evidence
 Laser = MITOCHONDRIAL improves and INCREASE ATP
Collage
Inflammation
Bacteria
Vasodilation
Alter nerve conduction
Soft tissue healing
Arthritis RA OA
Lymphedema
Carpal tunnel

Superficial conditions = lower doses

Contraindication
 DOOM 6
 Direct irradiation of eye
 Over thyroid
 Over hemorrhaging
 Malignancy
 <6 mo after radiotheray

PRECAUTIONS
PRE – LIES
Pre-treatment with 1+ photosensitizer
Low back or abdomen during pregnancy
Impaired sensation or mentation
Epiphyseal plates
Sensitivity to light

Wear eyewar

Must wait 2 weeks after steriods

TATTOOS increase temeratures
Skin sensitive for children and elderly

1. Blood-Flow Restriciton Training:

a. Within scope, application of external pressure over the extremities
b. Pressure = partial restriction to arterial BF and more significant affect venous
OUT FLOW
i. Lack O2 = hypoxia in muscle tissue
1. Blood pooling = increases intramuscular pressure with
contraction
2. A STYM : Less force and glides PARALLEL
3. I.A S TM (graston): causes Microtrauma; fibroblast activation , neuromodulation, inc
vascular response
a. Tissue turnover and REGENERATION
b. MORE FORCE and crosses friction to brake scar tissue
4. Dry needling:
a. Neurmuscular effects, pain, inc blood flow, inflammatory response, mm
relaxation
5. Cupping: stretches soft tissue = microcirculation
6. Percussion
  Remember to use all of the resources we have reviewd in class as study guides
(electricity questions, laser and light jeopardy, case scenarios, lab handouts)
o Know your waveforms
o Know the mechanism of action for the various types of electrical
modalities
o Contraindications and precautions are still a part of this exam

 Remember there are a couple of modalities that were not on your praftical that
are on this exam:
o Electricity for tissue healing: High volt (HVPC)
 Make sure to know the type of waveform and how polarity
works in regards to tissue healing
o Laser and light
 Make sure to know the mechanism of action for laser - what it
is impacting at the cellular level
o Special topics
 As we disussed in class, you don't need to know much from
this section except:

1. The general level of evidence for that modality (which has the highest leve?)
2. The basic mechanism of action for each modalitie (how is it proposed to work?)

You do NOT need to know things from the BFR protocol handout in lab that is for your
reference and future practice