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Samenvatting

Full summary Physical applications

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Complete summary of the courses, ppt and textbook in english all put together.












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Geüpload op
9 februari 2021
Aantal pagina's
67
Geschreven in
2020/2021
Type
Samenvatting

Voorbeeld van de inhoud

PHYSICAL APPLICATIONS: SUMMARY EPA



Examenverdeling
Schriftelijk examen (EPA + muscle stimulation + PA & CT Movant + E-health): 30%
Mondeling examen (EPA): 50%
Taak PDB: 15%
Taak JM: 5%


CHAPTER 1: PAIN DECREASING CURRENTS




Why PDC?
Given the final goal of a PT treatment: send the patient home cured or in a much better shape
PDC will allow us to achieve this goal:
o Easier
o Faster
o Cheaper
o With more comfort for the patient
Than without and in certain cases it will be the only treatment possible!

9 parameters, 2 current types (TENS, MET) and 3 levels = 7 decreasing mechanisms (see below)




1

,PHYSICAL APPLICATIONS: SUMMARY EPA


Electric current types and introductory concepts
1. Electric currents RK
Always answer 3 questions:
o What current?
o How do we set the parameters?
o What physiological effect have these currents?
 Self-study module and PPT answer these

Mostly common: TENS, MET, interferential current (IF), high-voltage (HV), diadynamic current
(DIA) and ultra-reiz current (UR)
Most efficient and useful: TENS and MET

The endorphin experiment:
S – M – N threshold
o Sensory threshold = level of first perception = ‘ik voel hem’
o Motor threshold = level of first perception of motor activity = ‘ik voel spier’
o Nocisensory threshold = level of pain intolerance

2. Analgesia and pain pathways
= pain relief

2.1 Pain Decreasing Mechanisms (PDM) RK
3 anatomical places
 Local/site of stimulation (peripheral effects)
 Dorsal column (spinal effects)
 Brain (central effects)

Local effects
1. Slowing down nerve conduction velocity
o TENS decreases conduction speed of the afferent nerve
o Less nociceptive stimuli will reach the spinal cord  pain relief
o Significant, but short effect (5min)

2. Local hyperemia
o Increased amount of blood under the contact surface of the electrodes
o Only by monophasic mA (strong effect) & uA (weak effect),
being: DIA UR APS MET
o Increased blood flow reaches skin (< 500%) and muscles (< 300%)
 more nutrients reach target site and more wastes to be washed away
o Increase of metabolism at electrode site  tissue healing effect  pain relief
o Constant ion transport of a direct current represents a threat to the cell  release of
inflammatory mediators  vasodilation

3. Reduction of substance-P
= Neuropeptide acting as a neurotransmitter
o Important element in pain perception
o TENS (all mA) is known to reduce substance-P

4. Tissue repair
o Only caused by MET and HV


2

,PHYSICAL APPLICATIONS: SUMMARY EPA

o Underlying effect not fully understood –categorized as cellular effects
o Tissue heals  cause of pain disappears  pain decreasing
o “gating” = the opening and closing of physiological channels in response to changes in
the membrane potential initiated by electrical stimuli
o MET can cause an opening in the ‘’voltage-sensitive channels’’
o MET: increase intracellular concentration of Ca and Na
= regulator of Ca and Na influx
o Changes in membrane potential  altered intracellular Ca-concentrations
o Voltage-gated Na-channels are responsible for the AP for nerve impulses  pain
decreasing effect from MET explained
o “Primary active transport” = cellular influence for transmembrane transport
o Transport protein guides substances through the membrane against an existing
electrical, chemical or pressure gradient. Energy = ATP (provided by metabolism)
o Study of Cheng et al (rats):
 ATP in skin under the influence of MET: 500% higher
 Peak values at 500 uA and decreased at 750 uA
 Uptake of GABA increased at 10 uA, drastic decrease at 750 uA
o Fibroblasts are sensitive to electrical stimulation: impact on collagen production
o Fibroblasts = important role in tissue repair  electrostimulation repairs tissue
o Other studies on p9, but not enough scientific background

Spinal effects
 Spinal pain modulation (SPM)
 “Gate control theory of pain”
o Nerve impulses reach thick and thin fibers from their receptors (each with their own
function)
o Both fibers activate the transmission cells (activated when a stimulus threshold is
reached)  pass information to the brain
o Both fibers also reach the substantia gelatinosainhibits activity in T-cells
 activity in thick fibers stimulates the SG
 activity in thin fibers inhibits the SG
 Result: a balance is created in both fibers  activating/inhibiting SG
 which will in turn inhibit or leave T-cells untouched
 Inhibited: the info can’t pass on to the brain
 Habituation to mild stimuli is regulated by this mechanism (thick f)
E.g.: you adjust to wearing skinny jeans, but not to sitting on keys Keys:
conduction through both fibers, this activity stimulates SG and T-cells  pass
nociceptive info to the brain about the keys
= outlined way in which the gate is kept open for painful stimuli!

 “Central control mechanism”
o Emotions can operate the gate from any part of the body
o This makes random motor activity possible, despite powerful pain stimuli
o TENS: good scientific and clinical evidence for the gate control mechanism
o MET: remains unclear whether mechanism works (effect seems minimal)


Central effects
 Central pain modulation (CPS)
 2 groups: ascending/descending and endorphins/enkephalins
 Ascending and descending pathways

3

, PHYSICAL APPLICATIONS: SUMMARY EPA

o TENS activate large diameter afferent fibers
o This afferent input  CNS  activates descending inhibitory system  reduces
hyperalgesia
o SO: descending inhibitory systems are activated by electrical stimulus of TENS

 Endorphins and enkephalins (opiates)
o Enkephalins: peptides produced by the body, strong analgesic effect
o Endorphins: more powerful pain-relieving effect, present in the pituitary gland in high
concentrations.
o β- endorphins have the strongest analgesic properties, next enkephalin and dynorphine.
Only active opiate-like factor in the body (runner’s high).
o TENS can trigger this mechanism by stimulating IIIb and IV-type afferents.
o Enkephalins: produced in the brain (encephalon) and have similarities in chemical
structure to morphine, storage is provided in the nerve endings
o Reverse the effect of endorphins  administering naloxone (opiate antagonist)  which
has no analgesic effect
o Release of endorphins after the pain-relieving effect  chemical changes in the peptide
chains  lose their analgesic, opiate-like effect  happens quite quickly with
enkephalins  Endorphins have a longer lasting effect




2.2 Introductory concepts related to pain
The following sections describe (pain)stimuli pathways from the skin to the brain. Along this
pathway, electric stimuli will have their effects.

 Stimulus response pathway
o Sensory stimuli in sensors  afferent peripheral nerve fibers, plexus and spinal nerve 
dorsal horn of the spinal cord  cells in different layers = laminae
o Stimulus ascends  thalamus and postcentral gyrus + frontal cortex and limbic system
 to provide info to the brain AND to be diverted to the motor ventral horn AND to the
sympathetic lateral horn  Motor ventral horn  α- and γ-motor neuron activity
o Spinal cord is divided into 10 laminae and 2 laterally lying structures that divide stimulus
over different segments
 In the laminae = so called gate control system

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