TENS Flashcards
Nociception (neural, mechanical)
- reception of signals in the CNS evoked by activation of specialized sensory receptors (nociceptors) that provide information about tissue irritation or damage
- May or may not lead to the experience of pain
Pain (neural, mechanical, behavioral)
- (perception of an) unpleasant sensory or emotional experience
- Associated with, or resembling that associated with, actual or potential tissue damage
- Can be highly subjective
Pain is always a…
personal experience that is influenced to varying degrees by biological, psychological, and social factor
can pain be inferred solely from activity in sensory neuron
absolutely not
How do people learn the concept of pain
through their life experiences
Although pain usually serves an adaptive role…
it may have adverse effects on function and social and psychological well-being
What is one of the several ways to express pain?
- verbal description
- inability to communicate does not negate the possibility that a human or a nonhuman animal experiences pain
Neural Factors: Acute Pain
- Promotes adaptation and appropriately contextualizing
- Movement planning, decision making
- Memory, learning, fear
- Affective/autonomic responses, concentration
- Reflexive actions, fear, coordination, gating
Patients with Persistent Pain
- Unclear relationship of pain and tissue damage / input
- Difficult to predict flare-ups
- Poor tolerance of normal therapeutic approaches
- Problems with physical and functional upgrading * Difficulty generalizing gains to other activities
Neural Factors: Persistent Pain
- Decreased tactile acuity
- Abnormal sensori-motor response, autonomic changes
- cognitive impairment, mental fog/fatigue
- Altered emotional processing
- Motor dyscontrol
Central Sensitization Pain Mechanism
- Altered cognition and interpretation of nociceptive signals.
- Pain alarm system on overdrive.
- Recruitment of sub-threshold inputs to nociceptors
- Hypersensitivity by changing the sensory response of normal inputs (including mechanoreception)
- Changes in properties of receptors in the periphery and neurons in CNS
- Pain no longer coupled with nociceptive input
Central Sensitization leads to
- Altered sensory processing
- Malfunctioning descending inhibition
- Increased activity of descending pain faciliatory pathways
- Increased efficacy in processing of incoming nociceptive stimuli (Temporal summation, long-term potentiation)
- Persons with persistent spinal pain, for example, show more brain activity in response to painful stimuli and have activity in regions normally not involved in pain sensation
the Affective Pain Mechanism
- Type and location of symptoms are less important
- Central pathways involved
- Related to negative emotions and perception
What is more important than type and location of systems in the affective pain mechanism
- Intensity and disability of musculoskeletal pain are determined more by treatable psychological and social factors than by pathophysiological processes
Affective pain mechanisms include
- Anxiety, depression
- Anger, blame
- Significant life-changing event (trauma, abuse)
- Ability to cope is important variable
The Motor Autonomic Pain Mechanism
- Autonomic (sympathetic / parasympathetic dysfunction) –> Can see lymphedema, skin coloration changes, hair loss, excessive sweating, changes in muscular tone
- Neuroplastic changes –> “brain smudging,’ Somatotopic representations are disrupted
Receptor types active in somatosensation
- cutaneous/subcut mechanoreceptors (touch)
- Thermal receptors (temperature)
- Nociceptors (pain)
- Muscle/skeletal mechanoreceptors (limb proprioception)
Cutaneous/subcut. mechanoreceptors (Touch)
- A alpha, A beta (large / medium and both are myelinated)
- Associated with specialized receptor
Thermal Receptors (temperature)
A delta, C
Nociceptors (Pain)
A delta, C
Muscle/Skeletal mechanoreceptors (limb proprioception)
A alpha, A beta, A delta
3 Harmful Stimuli Active Nociceptors
- Thermal
- Mechanical
- Polymodal
Harmful Stimuli - Thermal
- Activated by extreme temperature
- Small-diameter, thinly myelinated A delta that conduct signals at ~ 5-30 m/s
Harmful Stimuli - Mechanical
- Activated by intense pressure to skin
- Small-diameter, thinly myelinated A delta that conduct signals at ~ 5-30 m/s
Harmful Stimuli - Polymodal
- Activated by high intensity mechanical, chemical, or thermal stimuli
- Small diameter, unmyelinated C fibers, slow (< 1 m/s)
Projection of Nociceptive Afferents to Dorsal Horn of SC
- Projection neurons in lamina I (marginal layer)
- Lamina V neurons
Projection neurons in lamina I (marginal layer) receive
- direct input from myelinated A delta nociceptive afferent fibers
- indirect input from unmyelinated C fibers via stalk cell interneurons in lamina II (substantia gelatinosa)
Lamina V neurons receive
- Low-threshold input from large myelinated A beta fibers (mechanoreceptors)
- Direct and indirect input from A delta and C fibers
What mediates synaptic transmission between nociceptors and dorsal horn neurons?
chemical neurotransmitters
Major excitatory neurotransmitter
- Glutamate
- Evokes fast synaptic potentials in 2nd order neurons
what does release of peptide neurotransmitters cause?
- slow EPSP’s in dorsal horn neurons
- Substance P released from C fibers
- Neuropeptides (including Substance P) appear to enhance and prolong the actions of glutamate
- May be responsible for the unlocalized character of many pain conditions (i.e., no specific uptake mechanism)
What happens upon repeated application of noxious mechanical stimulation?
nearby nociceptors that were previously unresponsive to mechanical stimuli now become
responsive (area around the injury has a lower threshold)
What does injury or tissue damage release?
bradykinin and prostaglandins
(these activate or sensitize nociceptors)
- This activation of nociceptors = Release of Substance P = acts on mast cells = release histamine = directly excites nociceptors
Local Sensitization Response
- ATP, acetylcholine, and serotonin are released from damaged endothelial cells and platelets.
- They act indirectly on nociceptors by triggering release of bradykinin and prostaglandins
What is one of the most active pain-producing agents
Bradykinin
- activates A delta and C fibers
Activation of nociceptors also causes results in the release of what ?
- Substance P
What can Substance P elicit
calor, rubor, and tumor
- Neurogenic inflammation
What is substance P responsible for?
- axon reflex, a physiological process characterized by vasodilation in the vicinity of a cutaneous injury
= acts on mast cells = release histamine = directly excites nociceptors
Noxious stimulation can produce long term changes in what?
dorsal horn neurons
- changes in synaptic transmission via changes in physiological properties of the neurons
What occurs under conditions of persistent injury?
- C fibers fire repetitively (increased frequency of
firing), and the response of dorsal horn neurons increases progressively - This is termed “windup.” (WDR neurons can be “wound up” but in contrast, nociceptive specific neurons follow the typical response to an AP)
Centrally mediated hyperalgesia can lead to..
- Spontaneous pain via long-term changes in the response of dorsal horn neurons through mechanisms that are like those underlying the long-term potentiation of synaptic responses in many brain circuits.
- Said another way, this is a type of “memory” of the state of C fiber input –> This is central
sensitization.
How is there a transition from acute to persistent pain
- Nociceptive system is not static and there is a dynamic neural network constantly adapting
- Nociceptive system alters its response characteristics depending on prior experience to noxious activity
- Decreased withdrawal reflex threshold in patients with chronic pain (eg, whiplash; fibromyalgia specifically)
- Spinal cord neurons are sensitized without peripheral tissue damage (stimulation of tissues where there was no tissue damage)
Surpraspinal mechanisms for transitioning from acute to persistent pain
- Catastrophizing may enhance pain
perception –> Withdrawal reflex is modifiable based - Cortical reorganization
What is the most prominent ascending nociceptive pathway
Spinothalamic tract
what does the spinothalamic tract include?
- nociceptive - specific, thermosensitive, and wide dynamic range neurons in lamina I and V through VII of the dorsal horn
where do fibers cross in the spinothalamic tract
the midline the travel in anterolateral white matter
Where do fibers from spinothalamic tract terminate
central lateral nucleus and VPL and VPM of thalamus
function of spinothalamic tract
Since cells at the origin of this tract have
discrete, unilateral receptive fields, this pathway functions to localize painful stimuli
Where do the 2nd order neurons in the spinoreticular tract originate
- Lamina VII and VIII
- Complex, polysynaptic inputs
- Contradicting information on whether this tract
crosses or remains uncrossed. - Ascends in anterolateral quadrant of the spinal cord and terminates in reticular formation and thalamus
Function of spinoreticular tract
Since neurons at the origin of this tract
generally have large, bilateral receptive
fields, this pathway has been implicated
in the processing of diffuse, poorly
localized pain
Where do second order neurons of spinoparabrachial tract originate
Lamina I and V
where do a major portion of the spinoparabrachial tract fibers project
via anterolateral quadrant of the spinal cord to
the:
* Parabrachial nucleus of the pons with extensive
collaterals to the mesencephalic reticular
formation and periaqueductal gray matter.
* Projections to the amygdala (critical nucleus of
the limbic system)
Function of the spinoparabrachial tract
- Affective aspect of pain – regulation of
emotional states –> affective motivation responses; threat learning. - PBN role in circuit promoting windup
- Role in activating descending analgesic system
Spinohypothalamic Tract contains axons of neurons found in what spinal cord laminae
I, V, VII, VIII
Where do axons from spinohypothalamic tract project to?
hypothalamic nuclei that serve autonomic control
centers involved in the regulation of the neuroendocrine and cardiovascular responses that accompany pain syndromes
Is there a single area of the cortex that is responsible for pain perception?
Nope
somatosensory cortex neurons have ……
small receptive fields and may not contribute greatly to the diffuse perception of aches and pains that characterize most clinical syndromes
What do cingulate gyrus (part of limbic system) and insular cortex (internal body state and autonomic component of pain responses) contain?
neurons that are activated strongly and selectively by nociceptive somatosensory stimuli
What does pain result from?
the balance of activity in nociceptive and non-
nociceptive afferents
What do large diameter (A alpha, A beta) afferents modulate?
nociceptive projection neurons
Absence of A alpha and A beta =
perception of pain is not normal
what inhibits projection neurons?
stimulating sensory afferents
What did the balance between sensory afferents and projection neurons prompt?
the gate control theory
Gate Control Theory - C fiber activation:
- Excites projection neuron
- Inhibits interneuron
- Produces pain
Gate Control Theory - A beta AND C fiber activation:
- Aβ fiber excites interneuron
- Inhibits projection neuron
- Pain is reduced
So what is Gate Control Theory saying?
Non-nociceptive afferents “close” and nociceptive afferents “open a gate” to the central transmission of noxious input
Criticisms of Gate Theory in persistent pain
No brain, no inflammation, no immune function. Can’t explain complexity of persistent pain or alternative pains (e.g., phantom)
Brain stimulation producing analgesia
- Brain stimulation
- PAG (gray matter surrounding 3rd ventricle
and cerebral aqueduct - Profound / specific analgesia
- Still respond to touch, pressure in area
- Also blocks spinally mediated withdrawal
reflexes normally evoked by noxious stimulation - Exogenous opiate-induced analgesia involves the same pathway
What are the 3 most common of the 4 classes of opiate receptors in the brain
Mu, delta, kappa
3 major classes of endogenous opioid peptides
- Enkephalins (activate at both mu and delta receptors)
- Beta- Endorphins
- Dynorphins (mainly at kappa receptor)
- Enkephalin and Dynorphin in PAG, Raphe N, dorsal horn
- Endorphins in hypothalamus and locus ceruleus
Interaction of descending modulatory and ascending pain pathways
- Primary afferent terminates on 2nd order spinothalamic projection neuron
- Local enkephalin-containing interneurons exert pre and post synaptic inhibitory actions at primary afferent synapses
- Descending serotonergic brain stem neurons activate local opioid interneurons and also suppresses the activity of spinothalamic projection neurons
Sensory- level TENS (conventional)
- At site or related (e.g., acupuncture point)
- Stimulating large afferents such as A Beta (gate-control)
Motor Level E-stim for pain modulation
- More typically used for nonacute pain
- Muscle contraction at site or related to site (myotome)
- Longer lasting response to stim –> implicates endogenous opiate mechanisms
Noxious Level Stimulation
- Goal: produce a painful stimulus in or remote from the pain site.
- Low or high freqs.
- Long pulse durations
- With or without muscle contractions
- Higher stimulation levels = mass excitation of fibers in peripheral nerve
- Systemic release of endogenous opiates
- Endorphin-mediated mechanism?
- Typically, not your first choice for pain relief
