Pain modulation Flashcards
Duality of pain
- Physiological experience
- Psychological experience
Function of pain
- warning for withdrawl
- alerts that something is wrong
- protective function ( spasm)
Goals of pain treatment
- To resolve the underlying pathology causing pain
- to modify the patient’s perception of pain so as to allow them to participate in other PT interventions
- to allow the pt to maximize their functional abilities
categories of pain nociceptive: Somatic
Activation of nociceptors found in most body tissue
- respond to mechanical and chemical stimuli
- found in integument, arthromusculoskeltal systems
- caused by injury, disease, or surgical intervention
- often referred to as normal pain
- often treated with EPAs
categories of pain nociceptive: Visceral
Activation of nociceptors found in viscera
- Referred
- diffuse and poorly localized
- specificity: not all visera are sensitive to pain
- EPAs not effective
categories of pain neuropathic: Peripheral pain
disease associated with peripheral nerves
-often treated with EPAs
categories of pain neuropathic: Central pain
due to pathological functioning of the CNS
- often delayed as in stroke, MS, Parkinson’s
- Seldom treated with EPAs
categories of pain psychogenic
- originates from nonorganic sources
- associated with emotional, cognitive, and behavioral responses
- Not treated with EPAs
categories of pain carcinogenic
- Caused by cancerous pathology
- severe
- EPAs not effective
Types of pain
- Acute
- Chronic
- Referred
- Radicular
Acute pain
- time limited
- mediated through rapidly conducting pathways
- associated with increased sympathetic nervous system activity
- intensity: related to extent of tissue damage
- location- well localized and defined
- duration- as long as noxious stimulus persists
- serves as protective function
- may impair function
Acute pain treatment aimed to:
- Facilitate resolution of underlying disorder
- reduce inflammation
- modify the transmission of pain from periphery to CNS
Chronic pain
- duration: several months to years
- symptoms: similar to original symptoms
- history of many treatment failures
- history of many medications tried
- continued use of analgesics and tranquilizers despite no long term effects
- intensity: unbearable or incapacitating
- often seeking the “right treatment” to cure pain
- result
Chronic pain psychosocial changes
- Depression
- Disturbed sleep
- Altered moods
- weight changes
- decreased energy
- decreased physical, social, and recreational activities
- increased family stresses
- increased economic difficulties
Chronic pain psychosocial results from
changes in sympathetic NS, adrenal activity, reduced production of endogenous opioids, or sensitization of primary afferents
- increased sensitivity to both noxious (hyperalgesia) and non-noxious (allodynia) stimuli
- wind-up or central hypersensitization
Referred pain
Pain felt at a location distant from its source
-from a nerve to its area of innervation
- from one area to another derived from the same dermatome
- from one area to another derived from the same embrionic segment
Peripheral nerve pathways from different areas converge on the same area of the spinal cord
-synapse with the same second order neurons to ascent to the cerebral cortex
Referred Pain example
Pain is referred from the diaphragm to the tip of the shoulder-both areas initially develop in the neck region during embyological development
- both have efferent innervation from phrenic nerve
- both have afferent innervation to the second & fourth level of C-spine
Pain of visceral or musculoskeletal origin converging on sam neuron in spinal cord
- usually interpreted as musculoskeletal
- musculoskeletal more common thus brain learns that stimulus along this pathway is more likely to be musculoskeletal and distributed to musculoskeletal area
Radicular pain
- Originating from an irritated nerve root
- follows dermatomal reference
Danger alarm system
- Transduction-Danger receptors
- peripheral transmission
- modulation
- central transmission
- perception
- pain control theories
Transduction
Sensors-danger receptors
- in walls and at ends of neurons
- convey info to spinal cord
- can be specialized
- mechanical
- chemical
- temperature
Superficial peripheral sensory receptors
- Mechano
- Thermo
- Noci
Mechano receptors
- Meissner’s corpuscles-Pressure and touch
- Pacinian corpuscles- Pressure and touch
- merkle cells- skin, stretch, & pressure
- Ruffini endings- skin, stretch, & pressure
Thermoreceptors
- Cold receptors
- Hot receptors
- **Temperature and temperature change
Nociceptors
Free nerve endings- Pain
Deep peripheral sensory receptors
- Proprio
- Noci
Proprioceptors
- Golgi tendon organ: change in muscle length & muscle spindle tension
- Pacinian corpuscle: change in jt position & vibration
- Ruffini endings: jt end range/?heat
The danger alarm system transduction: Sensors (danger receptors)
Respond by opening
- allow + charged particles into neuron
- sets off AP
Can be opened or shut by chemicals
- pain meds closes sensor thus it cannot transmit impulses to spinal cord
- bee sting opens sensors thus floods spinal cord with impulses
-life of sensor is short (days)
- number and type of sensor is under direction of neuronal DNA in dorsal horn nuclei
- rate of production generally stable
- can change sensitivity of neuron if change rate of sensor production
The danger alarm system transduction: Nociceptor “danger receptor”
- free nerve endings involved in danger detection
- skin-cutaneous danger
- tendons & jts- somatic danger
- body organs- somatic danger
- Responds to all manner of stimuli
- if enough sensors are opened a danger message is sent to spinal cord
- high activation threshold
The danger alarm system: Peripheral transmission afferent nerve pathway
Part of neuron with cell body outside spinal column in dorsal root ganglion
The danger alarm system: peripheral transmission peripheral nerve afferent fibers
- beta fibers: 6-12 um diameter myelinated transmit impulses at >30 m/sec
- delta fibers- 1-6 um diameter myelinated, transmit impules @ up to 30 m/sec
- C fibers- 1 mm thick unmyelinated transmit impulses @ 1-4 m/sec
A-beta fibers
- first order afferents, myelinated
- large, myelinated, fast conducting
- low stimulation threshold
- location: skin
- info transmitted: touch, vibration, hair deflection
- originates in hair follicles, Meissner’s corpuscles, pacinian corpuscles, merkle cell endings, ruffini endings
A-delta fibers
- first order afferent, myelinated
- originate from warm/cold receptors, few hair follicles, and free nerve endings
- group III afferents
- noxious mechanical stimulus (pinch, prick,crushing)
- may transmit non noxious stimulus also
- large, myelinated, slower than A-beta
- quick onset, short duration
- well localized to area of injury
- not involved in emotional response
- not blocked by opiates
- info transmitted: touch, temp, pressure, pain
C-fibers
- first order afferent, unmyelinated
- 80% of afferent danger-transmitting fibers
- AKA: group IV afferents
- small, unmyelinated, transmit AP slowly
- respond to noxious levels of mechanical, thermal, and chemical stimulation
- result in sensation felt as dull, throbbing, burning, aching, tingling, tapping
- slow onset after initial stimulus
- long lasting emotionally difficult to tolerate
- diffuse locally
- can be accompanied by autonomic responses such as sweating, increase HR, BP, or nausea
- reduced by opiates, blocked by opiate antagonist naloxone
- location: muscle, skin
- info transmitted: pain, touch, temp, pressure, pain
Danger alarm system peripheral transmission: mechanical trauma
Activates both A-delta and C-fibers
Drop brick on foot
-immediate sharp sensation ( A-delta)
- produced by high intensity mechanical stimulus
-deep ache may develop that lasts hours (c-fibers)
-produced by chemical mediators of inflammation process
Danger alarm system central transmission: A delta fibers
Ascend in lateral spinothalamic tract and synapse with 3rd order neurons in thalamus, relay info to somatosensory cortex in postcentral gyrus
Danger alarm system central transmission: C-fibers
Ascend in anterior spinal thalamic tract and synapse in reticular formation and intralaminar nuclei of thalamus, relay info to association cortex
First pain pathway
- Frontal lobe>
- medial lemiscus in midbrain>
- Spinal nucleus of CN V>
- Dorsal column second order nueron
- lateral spinothalamic tract>
- 1st order neuron
Second pain pathway
- Dorsal root ganglion in spinal column>
- up paleospinothalamic, spinomesencephalic, and spinoreticular tracts (multisynaptic afferent systems)
- CNs V, IX, X>
- periaqueductal grey>
- frontal lobe
Danger alarm system central transmission: neurons that transmit pain
- NS: nociceptive specific
- WRD: wide range dynamic
Danger alarm system central transmission: spinothalamic tract
primary nociceptive pathway
- transmits type/location of pain
Danger alarm system central transmission: spinoreticular tract
Motivational, emotional, unpleasant aspect of pain
Danger alarm system central transmission: spinomesencephalic tract
Sensorimotor integration of pain
Danger alarm system central transmission: spinohypothalamic tract
Lymbic tract: autonomic responses associated with pain
Danger alarm system central transmission: sub-cortical centers
- reticular formation
- periaqueductual gray
- hypothalamus
- pitutiary
- thalamus
- limbic system
reticular formation
meidates autonomic and sensory functions
periaqueductual gray
directs descending inhibition
hypothalamus:
controls endocrine functions and vegetative state
pitutiary
master gland for endocrine system
thalamus
final gateway and relay center
limbic system
involved in emotional, motivational, and affective behavior
Danger alarm system central transmission: Somatosensory cortex
- Area of brain that identifies location of pain
- central processing center
- location and extent of danger associated with activation of somatosensory cortex
Danger alarm system central transmission: association cortex
- Responsible for affect that is associated with danger signals
- appraise the danger associated with the situation
- results in pain tolerance
Specificity theory
- Pain modulation theory
- sensation of pain depends on stim of specific nerve endings that are specialized for that sensation
- specific pain fibers are responsible for transmission of pain
- will always transmit the same sensation
- Von frey identified free nerve endings in skin that caused pain when stimulated
- However…
- sensation of pain does NOT have precise one to one relationship with type of receptor stimulated
- many types of stimuli can be perceived as painful
- pain can be modulated by input from the spinal cord or brain
Pattern theory
- pain mod theory
- senstation of pain results from appropriate intensity/frequency of stim of receptors that also respond to other stimuli like touch, pressure, temp
- temporal and spatial summation of impulses from periphery to cerebral levels determines perception of pain
- accounts for wide variety of stimuli can cause sensation of pain
- central influence of pain perception
- BUT:
- fails to consider role of specific identified receptors
- fails to account for affective or central pain mod
Peripheral pain modulation theory
- Desensitize peripheral receptors activated during inflammatory process
- bradykini, prostaglandin E2 and serotonin facilitate nociceptor sensitivity
- stein identified opioid receptors at peripheral nerve terminals
- effects most pronounced during inflammatory conditions
- non thermal US reduces pain during inflammatory stage
- MENS microcurrent electrical nerve stimulation desensitizes peripheral receptors
Gate control theory
- Melzak and wall 1965
- nerve impulses evoked by injury are influenced in the spinal cord by other nerve cells that act like gates
- pain sensation> balance of excitation & inhibition input on T-cells
- increased activity of nonnociceptor sensory afferents> presynaptic inhibition of T cells
- closes spinal “gate” to higher cerebral cortex centers> decreased sensation to pain
- enkephalin interneuron inhibits pain transmission in dorsal horn
Gate control theory mechanism
- IA, IIA, A-beta fibers stimulate T cells which cause second order wide dynamic range afferent. they also stimulate the spinal gate which releases enkephalon interneuron that stimulates T cells to release enkephalon to cause second order nociceptive afferent
- A-delta fibers and C-fiber nociceptors also stimulate T cell to release Enkephalon
Gate control theory influenced by phys agents
- electrical stimulation, massage, traction, compression> activate nonnociceptor sensory afferents ( low-threshold, large diameter, nonnociceptor sensory nerves)
- inhibits T cell activation in spinal cord
- Does NOT account for desending controls from higher brain centers
Supraspinal and Descending pain modulation
- uses feedback loops to inhibit pain transmission at dorsal horn
- results in release of endogenous opioids
- involves numerous nuclei in brainstem reticular formation including PAG and raphe nucleus
Endogenous opioid system
- 1973 disovered separate opiate binding sites in the CNS
- 1975 two peptides (met-enkephalin and luenkephlin) produced physiological effects similar to morphine
- bind specifically with opiate antagonist
- other similar peptides identified
- beta-endorphin, dynorphin A and B
Endogenous opioid system: opiopeptins
Control pain by binding with specific opiate receptors in the NS
- localized in many peripheral nerve endings
- identified in PAGM, raphe nucleus in brain stem> structures that induce analgesia
- inhibit release of substance P from C fiber terminals
- always have inhibitory effect
- presynaptic inhibition- suppress influx of calcium
- post synaptic inhibition-activate outflow of K+ current
- indirectly inhibit pain transmission by inhibiting release of GABA in PAGM and raphe nucleus
Motor pain modulation
- Used to enhance the production of endogenous endorphins in anterior pituitary
- low frequency (2-7 cps) high intensity stimulation of peripheral nn stimulates pituitary
- has stimulating effect on raphe nucleus and PAG region of midbrain
- end result: stimulation of descending pain control system in dorsal horn
Noxious pain modulation
- Stimulation of C-fibers activates PAG region
- second system activates the Pons
- end result is stimulation of descending inhibition system in dorsal horn
- long phase duration E-stim an dice can be used to activate this system
Neuromatrix theory
- Pain is multidimentional experience
- produced by characteristic patterns of nerve impulses generated by widely distributed nerve network in the brain
- determined by heredity
- included psychosocial factors, prior pain experience, cognitive and emotional experiences, general life stress
Nerve block pain modulation
- After nerve depolarization there is a refractory period where cell membrane cant depolarize
- application of medium frequency electrical current hyperpolarizes membrane further and blocks AP
- area between electrodes becomes temporarily anesthetized
Pain relies on context
- Splinter in finger
- ignition cues
- sensory cues that help start painful experience
- social consequences of being in pain
Altered danger alarms
Spinal cord
- adaptation begins within few secs
- danger messenger neurons increase sensitivity to incoming excitatory chemicals
- results in:
- hyperalgesia: that which hurts now, hurts more
- allodynia: that which did not hurt, now does
Pain assessment techniques
- VAS
- Pain charts
- McGill pain Questionnaire
- Activity pattern indicators profile
- numeric pain scales
- pressure algometry
Mcgill pain questionnaire (MPQ)
includes descriptors of sensory, affective, and evaluative aspects of pts pain
- sensory: temporal, spatial, pressure, thermal
- affective: fear, anxiety, tension
- evaluative: congnitive experience of pain in past and learned behaviors
- circles one word that best describes their pain
- sensitive to clinical changes
semantic differential scales
- word lists and categories that represent various aspects of pain experience
- Pt selects words that best describe pain experiences
- provide quantifiable data for intra and intersubject comparisions
Pressure algometry
-determines a pt’s force to pain onset
Pain management approaches: pharmacological
- modify inflammatory mediators peripherally
- alter pain transmission from periphery to cortex
- alter central perception of pain
- agent choosen depends on:
- cause of pain
- length of time meds will be needed
- side effects of meds
Systemic analgesics
- easy to administer
- inexpensive
- include NSAIDS, acetaminophen, opiates, and opiods, and antidepressants
NSAIDS
- have analgesic, anti-inflammatory, antipyretic, anticoagulant and possibly anticancerous effects
- can relieve mod severe pain of musculo origin especially if associated with inflammation
- inhibit conversations of arachidonic acid to cyclooxygenase and prostaglandins
- requires small dose to control pain vs inflammation
- reduce activity in C and A-delta fibers in acute and chronic jt inflammation
NSAID side effects
- GI irritation and bleeding
- dec platelet aggregation
- kidney damage
- bone marrow supression
- rashes and anorexia
NSAID drugs (types)
- Aspirin: 1st NSAID
- ibuprofin (motrin)
- naproxen sodium ( naprosyn, aleve)
- piroxicam ( feldene)
- celecoxib (celebrex) and rofecoxib (vioxx) cyclooxygenase type 2 inhibitors
NSAID how they work
- Original NSAIDS inhibited both cyclooxygenase subtype 1 and 2
- type 1> synthesized PGs that protect cells, maintain fx
- type 2> synthesized in response to cell injury, mediate pain, inflammation
- Cox 2 select drugs> inhibit synthesis of PGs in pain and inflammation
Acetaminophen
Tylenol
- effective for mild to mod severe pain
- has no significant antiinflammatory or anticoagulant effect
- can cause liver damage with prolonged usage
Opiates
- narcotics that contain opium or derivatives
types of opiates
- strong agonist (morphine)
- moderate agonist ( codeine)
- antagonists ( naloxone)
- mixed agonist/ antagonist ( butophanol)
how opiates work
- bind to opiate receptors
- blocked by naloxone
- mimic effects of endorphins and bind to opiate specific receptor sites in CNS
- may block pain by inhibiting release of presynaptic neurotransmitters and inhibiting interneuron activity early in nociceptive pathway
opiates adverse effects
- sedation
- mood changes
- confusion
- respiratory depression
- postural hypotension
- constipation
- nausea and vomiting
- tolerance and dependence
Antidepressants
- used in treatment of chronic pain
- amitryptiline (elavil) effects on sleep, nerve function, and mood
- pts with chronic pain and depression report higher levels of pain and pain related behaviors
Spinal analgeisa
Epidural or subarachnoid space
- opiates, local anesthetics, corticosterioids
- provides analgeisa to area innervated by segments of cord
- most effective if pain has a spinal distribution
- by-passes blood brain barrier increasing effectiveness and lessening side effects
spinal analgesia: Opiates
- Stimulate opiate receptors in dorsal horn of spinal cord
- fat soluble: rapid onset short duration
- water soluble: slow onset prolonged duration
Spinal analgesia: local anesthetics
- completely block nociceptive transmission
- increased concentrations can cause numbness and weakness
spinal analgesia: catabolic corticosteroids
- relieve pain due to inflammation of spinal nerve roots or surrounding structures
- prolonged use- osteoporosis, fat, muscle wasting
Local injections
- Relieving pain from local inflammation
- not after acute truama due to effect on healing by reducing inflammatory response
- prolonged use can cause tissue breakdown and deterioration
Phys agents directly:
- moderate release of inflammatory mediators
- modulate pain at spinal cord level
- altering nerve conduction
- increase endorphin levels
phys agents indirectly
Decrease sensitivity of muscle spindle system - reducing muscle spasm Vascularity (reduce edema and ischemia) - modify vascular flow - modify blood flow Help resolve underlying cause of pain
Moderate release of inflammatory mediators: cryotherapy
- reduces metabolic rate
- reduces production of serotonin, histamine, bradykinin, substance P, and prostaglandins
Moderate release of inflammatory mediators: sub thermal ultrasound
- alters cellular formation and release of inflammatory mediators
Modulate pain a Spinal cord level: stimulate large diameter afferent fibers
- TENS
- superficial massage
- analgesic balms
Modulate pain a Spinal cord level: decrease pain fiber transmission
- Cryotherapy
- ultrasound
- iontophoresis
- phonophoreis
Modulate pain a Spinal cord level: stimulate small diameter afferent fibers and descending pain control mechanisms
- Deep massage
- TENS (acupuncture like)
Modulate pain a Spinal cord level: stimulate release of beta endorphins through prolonged small diameter fiber stimulation
- TENS
- E-stim
Altering nerve conduction
- decreased nerve conduction is proportional to decrease in temp and duration of temp change
- 5 mins of cooling> reverses within 15 mins
- 20 mins cooling> needs greater than 30 mins to reverse
- cryotherapy
- ice pack, ice massage
increasing endorphin levels
E-stim
- certain parameters can control pain by stimulating release of opiopeptides at the spinal cord and higher centers
- pain relief reversed by naloxone
advantages to phys agents
- fewer and generally less severe side effects than meds
- pts do not develop dependency
- do not cause sedation
- many able to be applied independently
- may help remediate the underlying cause of pain
