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Flashcards in Chronic Pain Deck (23):

Protopathic pain fibers

A-delta fibers: myelinated, fast/well-localized pain
C fibers: slow secondary pain


Pain transduction pathway

-First order neurons in the periphery with cell bodies in spinal ganglion off posterior (most) nerve root (some enter ventral nerve root)
-Synapse with 2nd order neurons with cell bodies in dorsal horn of SC
-Synapse w/3rd order neurons w/cell bodies in thalamus


What is a rhizotomy?

Transection of dorsal nerve root off the spinal cord


Major lamina of dorsal horn

Lamina 1: somatic pain
Lamina 2: substantia gelatinosa (interneurons, important for modulating pain, especially somatic pain, densest opioid receptors)
Lamina 5: viceral pain


Opioid receptor activation

Hyperpolarizes (inhibits) both pre-synaptic 1st order neurons and post-synaptic 2nd order neurons
*Classic: endogenous opioids act pre-synaptically, exogenous opioids act post-synaptically


Nociceptor sensitization v inhibition

Nociceptor sensitization: decreasing threshold for activation; various mediators like PGs, histamine, bradykinin, substance P etc.
-prevent w/NSAIDs, ASA, APAP

Nociceptor activation: blockage of transmission w/LAs


Peripheral v central sensitization

Peripheral sensitization: occurs through chemically mediated (BK, PGs, sub P), heat, frequency of stimuli, etc
-leads to decreased threshold for nociceptor stimulation, decreased response latency, and after-discharge phenomenon (spontaneous firing after stimulus is gone)

Central sensitization: due to wind-up and sensitization of 2nd order neurons and WDRs through neurochemical mediators (CGRP, sP, etc), NMDA mechanisms, expansion of receptive field, and others



Small response from 1st order neurons leads to a larger response from 2nd order neurons
-NMDA agonism-->increased IC Ca2+-->neurochemical mediators that sensitize 2nd order neurons and increase aspartate and glutamate (which stimulate NMDA receptor)-->positive feedback loop


Neurogenic inflammation

"Triple Response"- flushing, edema, and sensitization of nociceptors


Mechanisms of neuropathic pain

-Reorganization and expansion of the receptor field for dorsal horn nociceptive (2nd order) fibers
-Spontaneous electrical conduction of a 1st order afferent neuron
-Short-circuits between nociceptive 1st order neurons and other types of neurons
-Decreased activity of supraspinal inhibitory pathways



MOA: alpha-2-delta calcium channel and NMDA receptor

Indications: diabetic neuropathy, post-herpetic neuropathy, fibromyalgia; and off label for phantom limb pain and spinal cord injury
*not effective for CRPS


Tramadol MOA

Agonist (weak, but specific) at mu opioid receptor
Increases serotonin release
Decreases norepinephrine uptake
Antagonizes NMDA
Agonist at VR1 (capsaicin) receptor


Which intervention during an episode of herpes zoster would most likely prevent post-herpetic neuralgia?

What are other treatments?

Epidural anesthesia- large sympathetic component

Tx: gabapentin, TCA, lidocaine patches, capsaicin, NSAIDs, opioids


CRPS pathophysiology progression

Acute pain with increased blood flow (edema, warm, red)-->vasospasm (cold, cyanotic)-->atrophy (osteoporosis, muscle wasting, ankylosing joints, contractors, glossy skin)


Early treatment of CRPS

Early: Sympathetic blocks (eg. stellate ganglion)- usually weekly, 3-12 injections
-gabapentin and TCAs often added but don't prevent progression w/o sympathectomy

Mainstay: PT

Last resorts: ketamine gtt, spinal cord stim


Phantom limb pain (PLP) treatment

Pregabalin (FDA approved), clonidine, NMDA antagonists, nerve blocks (avoid spinal anesthesia)


-anesthesia dolorosa

-Hypoalgesia: diminished response to a noxious stimulus
-Dysaesthesia: unpleasant sensation w or w/o stimulus
-Hyperalgesia: increased response to a noxious stimulus
-Hypoaesthesia: reduced epicritic sensation
-Paresthesia: abnl sensation w/o an apparent stimulus
-Anesthesia dolorosa: pain in an area that lacks sensation
-Allodynia: perception of non-noxious (epicritic) sensation as pain
-Hyperpathia: hyperesthesia, hyperalgesia, and allodynia w/overreaction and persistence of pain after the stimulus is gone



Stimulates large afferent epicritic fibers
Conduction blockage of small afferent pain fibers

Gate theory of pain: sending additional noxious or epicritic stimuli to the CNS, the original pain will no longer be as well perceived (rubbing a painful injury, "distracting pain"


Stellate Ganglion block

Anatomy-transverse process of C6 (Chassiaignac's tubercle)

Complications: Horner's syndrome (ptosis, miosis, anhidrosis, and nasal stuffiness), and hyperaemia and increased temp of ipsilateral arm


Celiac plexus
-vertebral level

Vertebral level: L1
MOA: upper abdominal sympathectomy (no motor fibers)


Trigeminal nerve block locations

-Gasserian nerve block- found in Meckel's cave
-Ophthalmic n: at supraoptic notch
-Maxillary n: between zygomatic arch and notch of mandible


Geniculate ganglion?

Cell bodies of afferent neurons of facial nerve
-blockade leads to Bell's palsy
-used to treat herpes zoster of facial nerve


Diabetic neuropathy EMG findings
-demyelination or axonal neuropathy

Diabetic neuropathy
-EMG: decreased amplitude, decreased conduction velocities, and prolonged latencies
-both demyelination and axonal neuropathy (mixed)

Demyelination: prolonged latencies and decreased conduction velocities

Axonal neuropathy: decreased amplitude