Modalities & Exercise Exam 2 Flashcards
Why Do We Need To Learn This?
Most TM applications are directed at relieving pain.
This information will make it make sense later.
Knowledge of all aspects of pain improves the ability to evaluate the individual on a multidimensional level and progress them through rehab safely.
Necessary to understand that not all pain experiences are related to an acute inflammatory response.
The whole evidence based practice thing .
What is Pain?
“an unpleasant physical and emotional experience which signifies tissue damage or the potential for such damage”
International Association for the Study of Pain (IASP)
Pain exists if the individual says it exists
Pain is essential to survival
Pain motivates the injured athlete to seek care and can help us make assessments
Etiological factors
factors that cause a condition
Sensory component
Rate your pain on a 1-10 scale, Visual Analog Scale, other pain scales
Pain Disability Index – comprehensive questionnaire
Oswestry Pain and Disability Index (p.98)
Validated?
Sensory + Affective-Motivational Component
Varies between individuals
Previous pain experiences, family experiences, cultural background, situation specific… these can create somatic markers (emotional memories)
Persistent pain outlasts its usefulness in identifying and injury, A-M aspect
Four types of peripheral sensory receptor
Special
Visceral
Superficial
Deep
Special Sensory Receptors
Sight Taste Smell Hearing Balance
little impact on the perception of (and response to) musculoskeletal pain
Visceral Sensory Receptors
Hunger
Nausea
Distension
Visceral pain
Superficial Sensory Receptors
AKA cutaneous receptors
“peripheral” because they are on the periphery (outside CNS)
Superficial Sensory Receptors
Mechanoreceptors
Stroking, touch and pressure
Some adapt rapidly (pressure and touch)
-Meissner’s corpuscles and Pacinian corpuscles (hair follicle receptors)
Some are more slowly adapting (pressure and skin stretch)
-Merkle cell endings and Ruffini endings
Superficial Sensory Receptors
Thermoreceptors
Temperature and temperature change
Slowly adapting, but discharge in bursts with rapid temperature change
Warm receptors stop discharging at temps that damage the skin
Cold receptors continue to discharge when tissue cooling is perceived as painful
Why don’t freezing injuries such as frostbite hurt as much?
Superficial Sensory Receptors
Nociceptors
Free nerve endings
Stimulated by: potentially damaging mechanical, chemical, and thermal stress
Sensitized by: prostaglandins, bradykinin, substance P, serotonin and others…
Contain the neurotransmitter L-glutamate which increases pain sensation
Deep Tissue Receptors
Muscle
Muscle Spindles and Golgi Tendon Organs (GTOs)
Sense changes in muscle length and tension
May also be sensitive to chemical stimuli
Joint Structures
Pacinian Corpuscles: Adapt rapidly and respond to changes in joint position and vibration
Ruffini Endings: Adapt slowly and are most active at the end ranges of joint motion
Both have Nocioceptors
Free nerve endings that say ‘Whoops, this is/that was too far!”
The Acute Pain Pathway
Ascending Pathways
Afferent Pathways
“First Pain”
Neocortical Tract
Fast, three-neuron pathway from the periphery (outside the CNS) to the cortex (area of the brain that identifies the location of pain)
Important Parts Nociceptor (skin, soft tissue, periosteum) Sensory nerve (first order neuron) T-cell (second-order neuron) Thalamus Sensory Cortex
Afferent Pathways
Impulses from sensory receptors are transmitted to higher brain centers by AFFERENT (OR SENSORY) NERVES
FIRST ORDER AFFERENT NERVE
In the periphery (outside the CNS)
Cell body in the DORSAL ROOT GANGLION
Synapses in the dorsal horn of the spinal cord
A-Beta Fibers (1st order afferent sensory nerve)
Originate from hair follicles, Meissner’s corpuscles, Pacinian corpuscles, Merkle cell endings, and Ruffini endings
Transmit info regarding touch, vibration and hair deflection
Large diameter and myelinated = FAST CONDUCTING
Relatively low threshold = EASILY STIMULATED
A-Delta Fibers (1st order afferent sensory nerve)
Get info from warm and cold receptors, a few hair receptors, and free nerve endings
Transmit info regarding touch, pressure, temperature pain
Free nerve endings primarily respond to pain: pinching, pricking, crushing
Small diameter and myelinated = SLOWER CONDUCTING
Higher threshold = NOT AS EASILY STIMULATED
C- Fibers (1st order afferent sensory nerve)
Smallest afferent peipheral nerves associated with pain
Also include efferent postganlionic fibers of the SNS
Primarily mechano and nocioceptors
A few are themoreceptors
Smallest diameter and NON-myelinated = SLOWEST CONDUCTING
Highest Threshold= REQUIRE MUCH HIGHER STIMULATION
where did that first order afferent sensory nerve synapse?
Dorsal Horn of the spinal cord
SECOND ORDER AFFERENT NERVE
Cell body is within the DORSAL HORN (grey)
2nd order neuron’s axon (white) makes up the ascending pathway
Synapses in the thalamus for both pleasant and noxious input
AKA “T-Cell” because they transmit info on
different tracts
T-Cells (2nd order neurons) cross the spinal cord (decussate) to transmit information up to the thalamus
Pain, temperature, touch, vibration and deep pressure
THIRD ORDER AFFERENT NERVE
Cell body is within the THALAMUS
Thalamus becomes a relay center
Sensory information is organized here
Facilitatory and inhibitory circuits established
Basically gets it ready to send to the somatosensory cortex of the brain
ALSO – the thalamus transfers input to the limbic system
Emotional, autonomic, and endocrine response to pain
Paleocortical Tract Pain
“Second Pain”
Slower and more complex than the acute pain pathway
Deals with the complex emotional components of pain
More intense stimuli activate polymodal nociceptors
These promote a more diffuse, unpleasant and persistent burning sensation that continues past the acutely painful stimulus
Peripheral Pain Modulation Techniques
GOAL: Desensitize the peripheral nocioceptors
ATCs try to counteract the effects of acute inflammation that sensitizes free nerve endings and peripheral nocioceptors
Bradykinin, prostaglandin E2 and serotonin facilitate nociceptor sensitivity
How can we do this?
Cryotherapy
Ice lessens the effects on chemical mediators and slow conduction velocity of all sensory input
Subsensory-level Estim and Non-thermal US
Microcurrent… proposed to affect pain modulation at peripheral level
Non-thermal ultrasound… empirical results
Descending Pathways
Any activity AFTER the cortex has received the input
These pathways ultimately have an excitatory or inhibitory action on new impulses being transmitted in the spinal cord
The Raphe Nucleus, Reticular Formation and PAG all have the potential to affect pain perception on the way back down
Raphe Nucleus
Reticular Formation
Controls level of arousal
Affects the individuals perception of well-being
In the brainstem
Controls autonomic functions and some motor functions
Helps provide collateral sensory signals to higher brain centers
When there is PAIN
PAG is activated and its network calms the person and helps filter pain signals by exciting the Raphe Nucleus and Reticular Formation
Pituitary gland can help regulate signals at spinal cord level which lessens impulses to the cortex
- The goal of pain management, through meds, modalities, or stress relief is to modulate the pain through these relay centers
Synaptic Transmission & Transmitter Substances
Synapse – where communication from one nerve fiber to another takes place
Transmitter Substance – a substance that may help or block transmission of neural impulses across a synapse
Glutamate and Substance P – facilitate/help
Beta Endorphins – inhibit/block
Gate
substansia gelatino
Supraspinal and Descending Pain Modulation
GOAL: to cause inhibitory signals to decrease the continued propagation of the pain message back to the spinal cord
Periaqueductal Gray (PAG) contains enkephalin-rich neurons that excite the Raphe Nucleus
Pharmacological Agents
Two techniques ATs can use to “recruit descending pain modulation”
Strong, pulsed motor stimulation
Noxious stimulation
Motor Pain Modulation
GOAL: to enhance the production of endorphins
No TENS treatment can eliminate pain, but can decrease it enough for therapeutic exercise
Theory: endogenous opioids (endorphins) production is enhanced by low-frequency, high-intensity stimulation of peripheral nerve fibers
Enough to evoke a muscular contraction
Rhythmic muscle contractions + A-delta fiber stimulation = enhancement of noxoius pain (descending tract) modulation
Noxious Pain Modulation
Electrical stim of the PAG matter of rat and human brains results in profound analgesia
Not something ATs do… obviously.
Basically,
Inhibitors are “turned on” by stimulation of C (pain) fibers in the affected region
ATs can do this… with a long phase duration
Point stimulator
Cryotherapy : CBAN
Burning and aching are caused by Cfibers and might evoke descending pain modulation
Nerve Block Pain Modulation
Law of Dubois Reymond
If stim is applied long enough to overcome capacitance, and applied rapidly enough to prevent accommodation then an action potential will occur
Wedinski’s inhibition
When the membrane cannot keep up and action potential failure occurs
Refractory period… if stimulation keeps occurring it actually hyperpolarizes the membrane and creates an inhibitory effect
Chronic Pain
Likely involves changes in nervous system operation
Nocioceptive system has “Plasticity” – ability to change
If these changes are permanent true chronic pain
Not all pain is permanent though!
Could truly be a biomechanical, structural injury
Could be psychological and able to be treated
Biomechanics
Failure to identify (AND TREAT!) real cause can explain persistent pain
Somatic Dysfunction
The biomechanics of the kinetic chain are altered by a state or dysfunction or malalignment
Address the underlying dysfunctions of the kinetic chain
Takes practice and skill!
Plan of Care
Persistent pain can be caused by_incomplete_ or inappropriate treatment plans
Rest-Reinjury Cycle
Patient education is key!
Have to earn their trust…
Reconditioning = careful control of exercise intensity, frequency, and duration
Rule: You should be able to do tomorrow what you did today
Be judicious with pallative care
The role of Therapeutic Modalities
Some electrical stimulation available
NMES
EMG Biofeedback
No direct modality application will retrain protective reflex responses and complex movements
Modalities can help decrease painful exercises aimed at restoring NM control
