Types of Pain Flashcards
What will determine what kind of pain you are having? What are the three overarching categories of pain?
the degree of injury, persistence of pain & adaptive/maladaptive responses you have in place
- nociceptive pain= noxious stimuli
- inflammatory pain= inflammation or tissue damage
- pathological pain= neuropathic pain or dysfunctional pain
What is acute pain?
nociceptive
in response to noxious stimulus
not chronic
activation of ascending pain pathways (pain inhibition from PAG & medulla)
termporary forms of peripheral & central sensitization
What is chronic pain?
inflammatory & neuropathic pain
inflammatory= stimulates processes that promote healing, prolonged stimulates peripheral & central neuronal excitability= increase sensitivity; pain usually stops once inflammation clears
neuropathic= intense non-damaging pain or damage/dysfunction of neurons in periphery/CNS= abnormal persistent pain transmission even after pain is gone
What is hyperalgesia?
increased pain sensitivity to nociceptors via decrease in threshold
primary= sensitization of nociceptive endings at site of injury
secondary= sensitization in CNS
central sensitization increases synaptic efficacy & reductions in inhibition= increase amplitude, duration & spatial extent of pain response
What is allodynia?
pain in response to non-nociceptive stimulus
Abeta or low-threshold Cs
involves central sensitization
nociceptive & mechanoreceptive pathways converge so that low threshold innocuous stimuli now can activate pain pathways
In normal sensations, nociceptors that respond to high intensity stimulate active what which lead to what? low threshold mechanoreceptors that respond to low intensity stimuli active what which lead to what?
nociceptors that respond to high intensity stimuli activate the central pathways that lead to pain
low threshold mechanoreceptors that respond to low intensity stimuli activate central pathways that lead to innocuous sensations
Central sensitization generates what two things?
hyperalgesia & allodynia
What is the mechanism of inflammatory pain?
substance P released induces vasodilation & release of inflammatory substances (bradykinin, histamine, ATP & PGEs) which activate peripheral nociceptors
TRPV1 protein ion channel that responds to heat is upregulated
Where is PGE2 from? What does it do?
synthesized from arachidonic acid by neurtrophils via Cox-2
activates kinases taht phosphorylates axonal membrane Na channels= increase sensitivity to noxious stimuli
What does prolonged pain produce?
NMDA Ca2+ channels (glutamate excitation) produces long term increases in dorsal horn neuron excitability via AMPA glutamate receptor upregulation
microglia sensitize spinothalamic neurons by releasing cytokines in response to NO, substance P, pathogens, etc
What are the two forms of neurpathic pain?
spontaneous pain: continous or paroxysmal burning, electric, tingling & shooting; caused by sprouting of axons & ephaptic communication
evoked: primary & secondary hyperalgesia plus allodynia (peripheral & central sensitizations)
Neural trauma increases primary neuron sensitivity to what neurotransmitters?
NE & EPI
cytokines from close by injured axons regulate adrenergic receptors; build up of NE/EPI triggers pain
In allodynia, with nerve trauma or overstimulation what happens to the different types of nerve fibers?
- Cs degenerate
- Abeta axons upregulate substance P (more SP= more pain) & sprout into lamina II where they innervate dorsal horn
- low threshold non-noxious tactile Cs become more sensitive rapidly
In hyperalgesia, what happens to the different types of nerve fibers?
- C afferents from viscera cause central sensitization of Abeta neurons in matter of mins
- after long time Abetas sprout & respond to cutaneous & muscle input as pain rather than normal tactile & proprioceptive inputs
What does central sensitization and prolonged pain cause?
ON cells are mediated by what neurotransmitters?
What does prolonged exposure to opioids cause?
descending axons from RVM ON cells sensitize DHNs in inflammatory & neuropathic conditions
shift from mostly OFFs to ONs= maintains central sensitization by facilitating pain transmission in dorsal horn
ONs mediated by CCK, glutamate, NE, & neurotensin
prolonged opioid exposure enhances CCKs ability to excite ONs
Nocebo stimulates CCK effect
What does opioid withdrawal cause?
hyperalgesia by ON cells in RVM
increases glutamate synaptic transmission & noradrenergic activity in RVM neurons
this leads to activation of descending facilitation= more pain specifically hyperalgesia
What is the reappraisal-emotional matrix made up of?
forebrain & amygdala
- cognitive functions depend on PFC & amygdala
- in negative emotional states increased activity in lateral orbitofrontal cortex augments nociceptive pain
The amygdala contributes to both _____ & _____ aspects of pain.
cognitive & emotional-affective
Amygdala receives info from where? chronic pain causes what? Where does the amygdala project pain to, to do what?
receives bottom up input from PB nucleus/thalamus & top down input from cingluate
chronic pain enhances excitability leading to central sensitization
amygdala projects to PAG to regulate pain sensitivity
What does the dlPFC do in relation to/with pain? what is the path?
emotional-decision making plus localization of acute pain
path: thalamus, primary & secondary somatosensory cortices & posterior insula
more active in homeostatic reglation of acute pain (pain inhibition) via descending pathways through PAG
What does the mPFC do in relation to/with pain? what is the path?
emotional, motivation & hedonic quality of perceived pain
path: amygdala, anterior insula & basal ganglia
more active in chronic neuropathic pain (pain enhancement) via descending pathways through PAG & ON cells of RVM
What does the mPFC respond to? What does the dlPFC respond to?
mPFC= severe pain & engages emotional-mentalizing region of brain into state of cont negative emotions
dlPFC= emotional-decision making (how to cope)
overall state of pain & suffering depends on their interaction & inhibition of e/o
What does low back pain cause in relation to the dlPFC
With chronic low back pain the dlPFC degenerates= permits heightened activity of mPFC & decreased ability in emotional-decision making
What does chronic back pain cause in relation to reduction in grey matter density? IBS? fibromyalgia, tension headaches?
low back pain: bilateral dlPFC & unilateral thalamus
IBS: insula & cingulate cortex
fibro & tension headaches: multiple regions
What does the migraine center trigger?
cortical spreading depression accompanied by oligemia, resulting in aura, including visual scintillations
pain fromsensitized perivascular afferent neurons which generate conscious pain via trigeminal pathways & stimulate parasymp reflex to vasodilate meningeal blood vessels
What does cortical spreading depression (CSD) cause the release of?
K+, H+, NO, arachadonic acid & PGE from pia whihc sensitizes perivascular trigeminal nerve afferents= PAIN
What prevent sensitization?
triptans: serotonin, which normally inhibits peptide release
triptans are 5HT (serotonin) agonists that alleviate migrain pain by stimulating 5HT receptors on bvs & nerve terminals
What is the only part of the brain that can feel pain?
dura mater!
due to distension of vasodilated meningeal vessels
What are the two mechanisms which can cause a migraine?
photophobia
ciliary muscle over contraction
What are the changes that are consistently identified in pts w/chronic pain?
anterior cingulate cortex, prefrontal cortex & insula show consistent changes decreased grey matter decrease in opioid receptor binding decrease in white matter integrity increase in inflammation in ACC/PFC
