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159 Cards in this Set

  • Front
  • Back
perception of an ordinarily non-noxious stimulus as pain
absence of pain perception
absence of all sensation
pain in an area that lacks sensation with or without a stimulus
unpleasant or abnormal sensation with or without a stimulus
dimished response to noxious stimulation (pinprick)
inceased response to noxious stimulation
increased response to mild stimulation
presence of hyperesthesia, allodynia, and hyperalgesia usually associated with overreaction, and persistance of the sensation after the stimulus
reduced cutaneous sensation (light touch, pressure, or temperature)
pain in the distribution of a nerve or a group of nerves
abnormal sensation perceived without an apparent stimulus
functional abnormality of one or more nerve roots
Nociceptive (bone, muscle, visceral)
caused by activation or sensitization of peripheral nociceptors (peripheral nerve endings)
Neuropathic (burning, tingling, pins and needles sensation)
caused by injury or acquired abnormalities of peripheral or central neural structures. (diabetes)
Describes the recognition and transmission of painful stimuli.
Stimuli generated from thermal, mechanical, or chemical tissue damage may activate nocioceptors, which are free afferent nerve endings of myelinated A-delta and unmyelinated C fibers.
free afferent nerve endings of myelinated A-delta and unmyelinated C fibers.
Nociceptors are
receptors that transduce noxious stimuli.
free nerve endings that sense heat, mechanical, and chemical tissue damage.
Respond to pinch and pinprick.
Silent nociceptors
Respond to inflammation
Polymodal mechanoheat nociceptors
most prevalent; respond to excessive pressure, extremes of temp (> 42C and < 18C), and alogens (pain producing substances).
pain producing substances
Protopathic sensation
noxious (pain) subserved by high-threshold receptors (very sensitive) conducted by smaller, lightly myelinated (Aδ) and unmyelinated (C) nerve fibers
Epicritic sensation
nonnoxious (not painful) light touch, pressure, proprioception, and temperature discrimination Characterized by low-threshold receptors Generally conducted by large myelinated nerve fibers
Gate Theory of Pain
Patrick Wall and Ronald Melzack (1965).
Pain transmission to the brain is blocked by “gates” located at the spinal cord level and the thalamus.
These gates open or close, either allowing or blocking pain impulses from registering in the brain.
The body may experience pain but the brain will not perceive it, if the gate is closed.
Summary: Gate Theory
The spinal cord and brain stem contain “gates,” which open or close.
Theorized: Large diameter fibers close gates while small diameter fibers open gates.
When there is no stimulation, the small and large fibers are silent; the gates are closed.
A Beta fibers
5-12 microns
Large, myelinated fibers.
Transmit impulses quickly.
Transmits sensations of touch, pressure and proprioception.
Carry sensations described as epicritic (non-noxious)
A Delta fibers
2-5 microns
Myelinated with lipid-like substance.
Transmit impulses fast.
Sense “sharp” and well-localized sensations. (needle poking your finger)
First pain or “Acute” pain
Carry sensations described as protopathic (noxious).
Warns you to react quickly.
C Fibers
0.4-1.2 microns (very small)
Transmit impulses slowly.
Sense dull, poorly localized sensations.
Second Pain or “Chronic” pain
Transmits protopathic sensations of pain, temperature, and touch.
Non-painful stimulation
Travels via large nerve fibers, A beta fibers; gates remain closed.
Painful stimulation
Travel via smaller diameter nerve fibers, A delta & C fibers; gates open and “painful sensation” is transmitted to the brain. (now you know you hurt)
Acute pain
Caused by noxious stimulation due to injury, a disease process, or abnormal function of muscle or viscera.
Associated with a neuroendocrine stress response (sympathetic nervous system stimulation) (kicked in the balls)
Self limited or resolves with treatment in a few days or weeks.
Two types: somatic ( either superficial or deep) or visceral
1) nociceptive stimulus (pinprick, acute burn, bee sting) ** skin
2) activation of nociceptors (activation of peripheral receptors, generation of action potentials, release of neurotransmitters from central terminals) ** dorsal root ganglion
3) activation of central pain pathways (dorsal horn to brainstem and thalamus)
Acute pain: Superficial
Due to nociceptive stimuli from skin, subcutaneous tissues, and mucous membranes.
Well localized
Described as sharp, pricking, throbbing or burning.
Acute pain: Deep somatic
Arises from muscles, tendons, joints, or bones.
Dull aching quality.
Less well-localized than superficial pain.
Acute pain: Visceral
Due to a disease process or abnormal function of an internal organ or its covering.
Presents as aching, dull and diffuse.
Poorly localized.
Refer to M & M, Table 18-2 to review patterns of referred pain.
Chronic pain
Neuropathic pain
Caused by an injury to the central nervous system that transmits pain.
Injury can be central or peripheral.
Described as burning, electrical and shooting.
Example: post-herpetic pain, diabetic neuropathy, or post surgical procedure
Sympathetically Maintained Pain
Complex Regional Pain Syndrome (CRPS)
Also called, Reflex Sympathetic Dystrophy
Nerve disorder that occurs at the site of injury, most often arms or legs.
Chronic condition characterized by severe burning pain, pathological changes in bone and skin, excessive sweating, tissue swelling and extreme sensitivity to touch.
Effects of Surgical Trauma
1) surgical trauma
2) Peripheral sensitization (primary and secondary hyperalgesia --> release of hydrogen ions, histamines, purines, leukotrienes, norepinephrine, K+ ions, cytokines, nerve growth factor, BK, PG's, 5-HT, neuropeptides
3) spinal wind up
4) central sensitization
Perception & Response to Pain
Four distinct processes
Transduction, transmission, interpretation, and modulation
Nociceptors are stimulated in skin and muscle.
A noxious, painful or tissue-damaging stimuli affects a peripheral sensory nerve ending.
The nerve is depolarized.
Generates electrical impulse.
The impulse is transmitted or carried throughout the nervous system.
The Spinothalamic Tract is the most important pathway for transmission
A subjective interpretation of pain by the patient.
How it feels to the patient.
Behavioral, psychological, and emotional factors are involved, which create an individualized perception of pain.
Modulation can either inhibit (suppress) or facilitate (aggravate) pain.
It is a neural response.(you can’t control it)
Peptides, amino acids and other mediators are released.
Chemical messages are released.
Endogenous mediators of inflammation
Prostaglandins (PGE1 > PGE2)
Bradykinin (peptide causes HR to slow down  a lot in the bowels) SNS you will have HR issues
Serotonin (found in brain and gut)
Lactic acid
Hydrogen ions
Potassium ions
Pain Pathways
Pain is conducted along three-neuron pathways from periphery to cortex (M&M, Figure 18-1).

First order neurons (FON) are located in the dorsal root.
Second order neurons (SON) are located in the dorsal horn.
Third order neurons (TON) are located in the inner chamber of the thalamus.
First Order Neurons (FON)
Located in the dorsal root ganglia.
Each neuron has a single axon which bifurcates, sending one end to the periphery and the other to the dorsal horn of the spinal cord.
Majority of FON send their axons into the spinal cord via the dorsal (sensory) spinal root.
Some unmyelinated fibers have been shown to enter the spinal cord via the ventral root.
This explains why patients still have pain after rhizotomy (transection of the dorsal nerve root).
Second Order Neurons (SON)
First order neurons synapse with second order neurons in the gray matter of the dorsal horn.
Spinal cord gray matter is divided into 10 lamina (Bror Rexed, 1952).
Lamina 1-6 make up the dorsal horn. These sites are where all afferent stimuli comes into the spinal cord.
Lamina 1-6 represent the principal site of modulation of pain by ascending and descending neural pathways.
Rexed laminae
The Rexed laminae comprise a system of ten layers of grey matter (I-X), identified in the early 1950s by Bror Rexed to label portions of the spinal cord.
Similar to Brodmann areas (defined based on its cytoarchitectonics, or organization of cells) Rexed laminae are defined by their cellular structure rather than by their location, but the location still remains reasonably consistent.
Rexed laminae II
Laminae II is also called the “Substantia Gelatinosa.”
It contains many “interneurons” (also called relay neurons, association neurons, connector neurons or local circuit neurons) - a multipolar neuron which connects afferent neurons and efferent neurons in neural pathways. (stop cocks)
It plays a major role in processing and modulating nociceptive (noxious) input from the periphery.
Major site of action for opioids.
Lamina III, IV & VI
receive non-nociceptive sensory input. (touch pain pressure)
Lamina VII
also called the intermediolateral column, contains preganglionic sympathetic neurons.
Lamina VIII & IX
Anterior horn (motor).
Lamina X
Very small neuron surrounding the central canal. Involved in pain, temp and visceral sensations.
Second Order Neurons (SON)
SON are either nociceptive or wide dynamic range neurons (WDR).
Nociceptive neurons
respond only to noxious stimuli; primarily located in Lamina I.
Wide dynamic range neurons (WDR):
respond to noxious (protopathic signals) and non-noxious stimuli (epicritic signals: light touch, temp, and proprioception.); most abundant in Lamina V. (INTERESTING TO US) these cause spinal wind up.
Wide Dynamic Range Neurons (WDRN)
These neurons can cause “spinal wind up” or “ratchet up” stimulation associated with pain.
After repeated stimulation, WDRN can increase their firing rate without having an increase in intensity from the stimulation.
Increased response results from the same amount of stimulus.
Continuous spontaneous firing occurs even after the stimulus is stopped or removed
mastectomy patients having pain two years later is from spinal wind up. What use to cause pain, now causes 4x the amount of pain. Lamina V involved.
1) pain signals in peripheral sensory nerve --> wind up
2) goes to the thalamus
3) periaqueductal grey matter --> descending inhibition down the spinal cord
Spinothalamic Tract
Major pain pathway.
Axons of the SON cross the midline to the contralateral side of the spinal cord before they form the Spinothalamic Tract.
Fibers leave the main pathway and enter the recticular formation, raphe magnus and periaqueductal grey matter (response to pain).
Spinothalamic tract is divided into lateral and medial tracts.
Lateral Spinothalamic Tract
Referred to as the “neospinothalamic tract”
“Neo” means “new.” evolved over time
Projects into the posterior lateral portion of the thalamus.
Lateral spinothalamic tract carries pain and temperature up to the brain.
Carries discriminative aspects of pain, such as location, intensity, and duration. Allows us to identify what pain sensations our patients are feeling.
I- marginal
II and III- gelatinosa
IV, V, VI- nucleus proprius
Medial Spinothalamic Tract
Referred to a paleospinothalamic tract
“Paleo” means “older.”
Projects into the medial thalamus.
Mediates the autonomic and unpleasant emotional perceptions of pain. Remembers the pain.
Alternative Pathways
Some tracts mediate autonomic responses to pain.
Some tracts activate emotional behavior to pain.
Ascending Sensory pathway
Also called, the dorsal lemniscal system.
Also called, the posterior column-medial lemniscus pathway .
Also called, the dorsal column-medial lemniscus (DCML) pathway.
A sensory pathway responsible for transmitting fine touch, vibration and conscious proprioceptive information from the body to the cerebral cortex via the Cuneatus and Gracilis tracts (toSensory information ascends on the same side before crossing over in the brainstem to the contralateral thalamus.
SSEPs (Somatosensory Evoked Potentials) monitor the ascending sensory pathway.
Up and then it crosses over.
Make friends with these people.
Amplitude and latency everything but opioids effect these.
Some use N2O some don’t.
uch, pressure, vibration).
DCML, touch, pressure and position
. Spinothalamic, skin temp and pain and is a little more slower.
Descending Tracts
corticospinal, or pyramidal tracts, and the extrapyramidal tracts.
The pyramidal tracts descend directly without synaptic interruption, from the cerebral cortex to the spinal cord.
Dorsolateral funiculus
descending tract that modulates pain.
Action potentials in this tract activate the enkephalin-containing neurons of the substantia gelatinosa, which diminish the transmission of pain. (runner’s high)
Stimulation of several areas in the brain (periaqueductal gray, reticular formation, nucleus raphe magnus) activate descending inhibitory pathways. (brains attempt to control the stimulus that we are feeling)
Descending Tracts
These pathways modulate the incoming stimulus at the dorsal horn.
These areas in the dorsal horn contain high concentrations of endogenous opioid transmitters, including endorphins & enkephalins, which inhibit the incoming pain message.
raphespinal, reticulospinal,
A posterior left-sided rhizotomy is performed on your patient:
Sensations carried in the spinothalamic tract (i.e., pain and temperature) would be lost on the opposite side from the dermatomes at, and below, the level of the rhizotomy.
If the right dorsal lemniscal tract is severed, which senses are lost?
Touch, pressure and vibratory senses would be lost from the right (same side of the body).
If the spinothalamic tract is severed at C2 on the right, what will happen?
Loss of pain and temperature transmission on the left side of the body at and below the level of the lesion.
If the left lateral spinothalamic tract is severed at C3, which sensations are lost?
Pain and Temp sensations on the right side of the body, at and below, C3.
Intergration : Sympathetic and Motor systems
Somatic and visceral afferents are connected to the skeletal motor and sympathetic systems in the spinal cord.
Afferent dorsal horn neurons synapse with anterior horn motor neurons.
Responsible for reflex muscle activity associated with pain.
Synapses between afferent nociceptive neurons and sympathetic neurons result in reflex sympathetically mediated vasoconstriction, smooth muscle spasm, and the release of catecholamines.
Third Order Neurons (TON)
Second order neurons synapse with third order neurons in the thalamus
Sends fibers to the somatosensory areas of the cortex.
Somatosensory areas are responsible for evoked potentials, the electrical signals generated by the nervous system in response to sensory stimuli.
Chemical mediators of pain
There are over 15 different amino acids, peptides and chemicals that act as neurotransmitters in the pain process.
Most neurons contain more than one neurotransmitter that is released at the same time. Anyting that effects pain by either inhibiting or stimulating it. Ex bradykinin, histamine, etc…
Excitatory pain-modulating neurotransmitters
Vasoactive intestinal polypeptide
Gastric-releasing peptide
Substance P
The most important excitatory peptides
Substance P (pain) and calcitonin gene related peptide (CGRP). (CGRP is a powerful arteriolar vasodilator.)
most important excitatory amino acid.
Glutamate is the most important excitatory amino acid. Transmits pain impulses. Binds to receptors and causes changes in sodium ion channels. (can either increase or decrease the rate of transmission)
Inhibitory pain-modulating neurotransmitters
Chemical mediators of pain (also called alogens)
Substance P
Substance P
11-amino acid peptide.
Synthesized and released by FON, both peripherally and in the dorsal horn.
Facilitates ascending transmission in pain pathways.
Sensitizes nociceptors. (this is not good)
Causes a release of histamine from mast cells.
Causes a release of serotonin (5-HT hydroxytryptamine) from platelets.
Potent vasodilator.
Chemoattractant for leukocytes.
Just keeping your patient light does a whole lot of stuff as shown by this side
Modulation of Pain
Occurs peripherally at the nociceptor, in the spinal cord, or in supraspinal structures.
Modulation can either inhibit (suppress) or facilitate (aggravate) pain.
Supraspinal structures fancy word for brain. Specifically the limbic the thalamus and the hypothalamus
Peripheral Modulation
Nociceptors become oversensitized after repeated stimulation.
Sensitization: enhanced response to noxious stimuli.
Newly-acquired responsiveness to a wider range of stimuli, including non-noxious stimuli.
Two types of peripheral modulation
Primary hyperalgesia
Primary happens when it is damaged and at the site.

Secondary hyperalgesia
Primary Hyperalgesia
Hyperalgesia: increased response to noxious stimulation.
Nociceptor sensitization usually occurs from injury or heat.
Results in a decrease in threshold and an increase in the frequency response to the same stimulus intensity. (repeated stimulus that now it hurts worse)
Spontaneous firing occurs even after the cessation of the stimulus.
Primary Hyperalgesia
Primary hyperalgesia is mediated by the release of alogens from damaged tissues, which contribute to inflammation and associated sensitivity and pain.
Histamine is released from mast cells and platelets.
Bradykinin is released from tissues and causes increased vascular permeability, promotes vasodilation, induces leukocytes, activates nocioceptors, and are potentiated by prostaglandins.
Prostaglandins are produced following tissue damage.
Secondary Hyperalgesia
Neurogenic inflammation.
Triple response: Redness, edema, and sensitization to noxious stimuli.
Occurs due to the release of prostaglandins and CGRP (calcitonin gene related peptide) from collateral axons of the afferent neuron.
Initially injured.
Potent vasodilators.
Intensify the effects of histamine, serotonin and bradykinins. (synergistically)
Cause increased permeability of blood vessels.
Lead to formation of substance P.
How are prostaglandins formed?
Tissue damage.
Phospholipase A2 enzyme, which is present in cell membranes, is stimulated by tissue damage.
Activation of phospholipase A2 causes release of arachidonic acid from the phospholipid cell membrane.
Two reaction pathways are catalyzed by the enzymes cyclooxygenase and lipoxygenase.
converts arachidonic acid to prostaglandins and prostacyclins , which potentiates the edema from bradykinin.
ASA, NSAID, and COX inhibitors inhibit cyclooxygenase.
Lipoxygenase pathway
converts arachidonic acid to leukotrienes, which cause increased vascular permeability and release of leukocytes.
Central Modulation
Exaggerated pain sensation (real but way more than we think is appropriate)
Facilitation: Central sensitization
Inhibition: Segmental and Supraspinal (these can occur to decrease it)
Wind-up and sensitization of second order neurons:
WDR neurons increase their frequency of discharge with the same stimuli and exhibit prolonged discharge even after stimulus has stopped.
Receptor field expansion
adjacent neurons become responsive to stimuli.
Facilitation of Central Sensitization
Wind-up and sensitization of second order neurons: WDR neurons increase their frequency of discharge with the same stimuli and exhibit prolonged discharge even after stimulus has stopped.
Receptor field expansion: adjacent neurons become responsive to stimuli.
Hyperexcitability of flexion reflexes. Spindles contracted and they can’t relax or straighten out.

When someone loses a limb and they still feel it.
Causes of Facilitation
Neurochemical mediators (i.e., prostaglandins, CGRP, glutamate, kinins, and aspartate) cause membrane changes and changes in intracellular calcium levels.
Glutamate and aspartate play an important role in spinal wind-up via activation of N-methyl-D-aspartate (NMDA) and non-NMDA receptors.
Results in increases in calcium concentration in spinal neurons, which eventually results in a release of prostaglandins.
Transmission of nociceptive input in the spinal cord can be inhibited by activity in the cord itself, as well as by descending activity from the supraspinal centers.
Segmental inhibition
A fibers serving epicritic sensation inhibit WDR neurons and spinothalamic tract activity (i.e., the Gate theory.) gates are shut no message gets to the brain and you don’t hurt.
Glycine and gamma aminobutyric acid (GABA) are amino acids that function as inhibitory neurotransmitters.
Inhibition of Glycine and GABA causes facilitation of WDR neurons.
Supraspinal Inhibition
Several supraspinal structures send fibers down the spinal cord to inhibit pain in the dorsal horn.
Impulses arising in the periventricular and periaquaductal grey are transmitted through the nucleus raphe magnus to the substantia gelatinosa (lamina II) by way of the descending dorsolateral funiculus.
Limbic, hypothalamus, and thalamus, mu, kappa, and delta but primary is Mu1 in the brain. Doesn’t take away the pain but alters the patient’s response to the pain. (opioids , knee is smashed up, they just don’t care about it)
Supraspinal Inhibition
Enkephalins (may be considered the gate in the gate theory), endorphins, dynorphins, GABA, norepinephrine, oxytocin (bond with their babies, and also causes the uterine contractions and to let down the milk) and relaxin are inhibitory neurotransmitters
These molecules bind to opioid receptors and decrease the release of substance P, resulting in decreased pain.
Neural Blockade
Local anesthetics (LA) play a major role by manipulating the sympathetic system and its pathways.
Neuraxial administration of LA-opioid mixtures ensures better preservation of pulmonary function, earlier ambulation, earlier physical therapy and lowers the risk for postoperative venous thrombosis.
Pre-emptive analgesia ensures a smoother transition following surgery or manipulation.
Chronic Pain Management (CPM
Diagnostic & therapeutic neural blockade
Neural blockade with local anesthetics are useful in delineating pain mechanisms.
Facilitates evaluation of the sympathetic nervous system.
Pain relief following diagnostic neural blockade is favorable, indicating relief will be successful.
Chronic Pain Management (CPM)
Therapeutic adjuncts
include psychological interventions, physical therapy, acupuncture and electrical stimulation
TENS or transcutaneous electrical nerve stimulation
SCS or spinal cord stimulation
Intracerebral stimulation
Somatic Blocks for CPM
Trigeminal nerve blocks
Facial nerve blocks
Glossophayngeal blocks
Occipital nerve blocks
Phrenic nerve blocks
Suprascapular nerve blocks
Cervical paravertebral nerve blocks (would be useful in the OR)
Sympathetic nerve blocks for CPM
Cervicothoracic (Stellate) block
Thoracic sympathetic chain block
Celiac plexus block
Splanchic nerve block
Lumbar sympathetic nerve block
Hypogastric plexus block
Ganglion impar block
Additional methods of neural blockade for CPM
Differential neural blockade
Radiofrequency ablation
Alcohol & phenol neurolytic blocks
What effects are attributed to Mu-1 receptors?
Supraspinal analgesia, decreased heart rate, euphoria, and itching.
What effects are attributed to Mu-2 receptors?
Spinal analgesia, respiratory depression, and addiction.
Adjuvant agents
Adjuvant agents include antidepressents, anticonvulsants, neuroleptics, corticosteroids, adrenergic agonists, and botulinum toxin.
Alternative methods of treatment include psychological interventions, physical therapy, acupuncture or acupressure, electrical stimulation and Child Life therapy.
INDICATIONS: trigeminal neuralgia and intractable cancer pain in the face
PERFORMED ON: gasserian ganglion itself, one of the major divisions (opthalmic, maxillary, or madibular) or one of the smaller branches
ANATOMY: rootlets of CNV arise from the brain stem and join one another to form a crescent-shaped sensory (gasserian) ganglion in Meckel's cave. Most is invested with a dural sleeve. The three subdivisions of the trigeminal nerve arise from the ganglia and exit the cranium separately.
through the superior orbital fissure
(part of the trigeminal nerve block)
cranium via the foramen rotundum to enter the pterygopalatine fossa, where it divides into its various branches.
(part of the trigeminal nerve block)
the foramen ovale, after which it divides into an anterior trunk, which is mainly motor to the muscles of mastication, and a posterior trunk, which further divides into the various sensory branches.
(part of the trigeminal block)
Horner's syndrome, and motor block of the muscles of mastication. The potential for serious hemorrhage is greatest for blockade for the maxillary nerve. The facial nerve may inadvertently be blocked.
INDICATIONS: relieve spastic contraction of the facial muscles and to treat herpes zoster affecting this nerve.
ANATOMY: the facial nerve exits the cranium through the stylomastoid foramen, where it can be blocked. A small sensory component supplies special sensation (taste) to the anterior two-thirds of the tongue and general sensation to the tympanic membrane, the external auditory meatus, soft palate, and part of the pharynx.
COMPLICATIONS: if the needle is inserted too deeply past the level of the styloid bone, the glossopharyngeal and vagal nerves may also be blocked.
INDICATIONS: used for patients with pain due to malignant growths at the base of the tongue, the epiglottis, and palatine tonsils. Also used to distinguish glossopharyngeal neuralgia from trigeminal and geniculate neuralgia.
ANATOMY; exits from the cranium via the jugular foramen medial to the styloid process and courses anteromedially to supply the posterior third of the tongue, pharyngeal muscles, and mucosa. The vagus and spinal accessory nerves also exit the cranium via the jugular foramen and descend alongside the glossopharyngeal nerve.
COMPLICATIONS: dysphagia and vagal blockade resulting in ipsilateral vocal cord paralysis and tachycardia. Block of the accessory nerve and hypoglossal nerves causes ipsilateral paralysis of the trapezius muscle and the tongue, respectively.
INDICATIONS: patients with occipital H/A and neuralgias
ANATOMY: greater occipital nerve is derived from the dorsal primary rami of the C2 and C3 spinal nerves, whereas the lesser occipital nerve arises from the ventral rami of the same roots.
INDICATIONS: may provide relief for pain arising from the central portion of the diaphragm. It can also be useful in patients with refractory hiccups (singultation).
ANATOMY: arises from C3-C5 nerve roots at the lateral border of the anterior scalenus muscle.
COMPLICATIONS: pulmonary compromise may occur in patients with preexisting lung disease or injury. Simultaneous bilateral phrenic nerve block should never be performed.
INDICATIONS: useful for painful conditions arising from the shoulder (most commonly arthritis and bursitis)
ANATOMY; major sensory nerve of the shoulder joint. It arises from the brachial plexus (C4-C6) and passes over the upper border of the scapula in the suprascapular notch to enter the suprascapular fossa.
COMPLICATIONS: pneumothorax if the needle is advanced too far anteriorly. Paralysis of the surpraspinatus and infraspinatus muscles can be troublesome.
INDICATIONS: diagnostic with pain coming from the cervical spine or the shoulder
ANATOMY: cervical spinal nerves lie in the sulcus of the transverse process of their respective vertebral levels. Cervical spinal nerves exit above their respective vertebral levels (unlike the rest which exit inferior to their respective levels)
COMPLICATIONS: unintentional intrathecal, subdural, or epidural anesthesia at this level rapidly causes respiratory paralysis and hypotension. Horner's syndrome, as well as blockade of the recurrent laryngeal and phrenic nerves.
INDICATIONS: anesthetizes both the dorsal and ventral rami of spinal nerves. Useful in patients with pain originating from the thoracic spine, thoracic cage, or abdominal wall, including compression fractures, proximal rib fractures, and acute herpes zoster. Must be used for blockade of upper thoracic segments, because the scapula interferes with the intercostal technique at these levels.
ANATOMY: each thoracic root exits from the spinal canal just inferior to the transverse process of its corresponding spinal segment.
COMPLICATIONS: most common is pneumothorax, sympathetic blockade and hypotension may be obtained if multiple segments are blocked or a large volume is injected at one level. CXR is mandatory afterward to r/o pneumothorax.
INDICATIONS: useful in evaluating pain due to disorders involving the lumbar spine or spinal nerves.
ANATOMY: lumbar spinal nerves enter the psoas compartment as soon as they exit through the intervertebral foramina beneath the transverse process. This compartment is formed by the psoas fascia anteriorly, the quadratus lumborum fascia posteriorly, and the vertebral bodies medially.
COMPLICATIONS: unintentional subarachnoid, subdural, or epidural anesthesia
INDICATIONS: may establish the contribution of lumbar facet (zygapophyseal) joint disease in back pain. Corticosteroids are commonly injected with the local anesthetic when the intraarticular technique is chosen.
ANATOMY: each facet joint is innervated by the medial branches of the posterior primarry division of the spinal nerves above and below the joint. Every joint is supplied by two or more adjacent spinal nerves. Each medial branch crosses the upper border of the lower transverse process running a groove between the root of the transverse process and the superior articular process.
COMPLICATIONS: injection into a dural sleeve results in a subarachnoid block, whereas injection near the spinal nerve root results in sensory and motor blockade at that level. Large injections can cause rupture of the joint capsule.
INDICATIONS: useful in diagnosis and treatment of pelvic and perineal pain. Blockade of the S1 spinal root can help define its role in back pain.
ANATOMY: five paired sacral spinal nerves and one pair of coccygeal nerves descend in the sacral canal, forming the cauda equina. Each then travels through its respective intervertebral foramen. The S5 and coccygeal nerves exit through the sacral hiatus.
COMPLICATIONS: nerve damage and intravascular injection
INDICATIONS: perineal pain
ANATOMY: arises from the S2-S4 and courses between the sacrospinous and the sacrotuberous ligaments to reach the perineum.
COMPLICATIONS: unintentional blockade and intravascular injection are common complications
subarachnoid, epidural, and paravertebral. These block both somatic and sympathetic fibers.
INDICATIONS: reflex sympathetic dystrophy, visceral pain, acute herpetic neuralgia, postherpetic pain, and peripheral vascular disease.
CHARACTERIZED by unaltered somatic sensation but loss of sympathetic tone as evidenced by increased cutaneous blood flow and temp. Other tests include loss of the skin conductance (sympathogalvanic) and sweat response (ninhydrin, cobalt blue, or starch tests) following a painful stimulus.
INDICATIONS: head, neck, arm, and upper chest pain. Blocks the upper thoracic as well as all cervical ganglia. Injection of large volumes >10 ml often blocks down to T5 ganglia.
ANATOMY: sympathetic innervation of the head, neck, and most of the arm is derived from four cervical ganglia. The largest is the stellate ganglion which usually represents a fusion of the lower cervical and first thoracic ganglia. The sympathetic supply to the arm in some persons may originate from T2-T3 (kuntzs nerves) that join the brachial plexus high in the axilla, these nerves may be missed by a stellate block but not by an axillary block. The stellate (where u inject) lies posterior to the origin of the vertebral artery from the subclavian artery, anterior to the longus colli muscle and the first rib, anterolateral to the prevertebral fascia, and medial to the scalene muscles.
COMPLICATIONS: hematoma, pneumothorax, epidural anesthesia, brachial plexus block, hoarseness due to blockade of the recurrent laryngeal nerve, and rarely, osteitis or mediastinitis following esophageal puncture.
ipsilateral ptosis, meiosis, enophthalmos, nasal congestion, and anhidrosis of the neck and face.
INDICATIONS: usually not used b/c the sig risk of pneumothorax
-the thoracic sympathetic ganglia lie just lateral to the vertebral bodies and anterior to the spinal nerve roots.
INDICATIONS: pain arising from the abdominal viscera, particularly abdominal malignant growths. Usually blocks the lumbar sympathetic chain.
ANATOMY: vary, generally clustered at the level of L1, posterior to the vena cava on the right, just lateral to the aorta on the left, and posterior to the pancreas.
COMPLICATIONS: most common is postural hypotension, which is largely due to blockade of the lumbar sympathetic chain.
INDICATIONS: less likely to block the lumbar sympathetic chain and req < anesthetic volume.
ANATOMY: 3 groups of splanchnic nerves (greater, lesser, and least) arise from the lower seven thoracic sympathetic ganglia on each side and descend alongside the vertebral bodies to communicate with the celiac ganglia.
COMPLICATIONS: hypotension and possible injuries to the azygos vein on the right or the hemiazygos vein and the thoracic duct on the left.
INDICATIONS: painful conditions involving the pelvis or the lower extremities, and possibly in some patients with peripheral vascular disease.
ANATOMY: lumbar sympathetic chain contains 3-5 ganglia and is a continuation of the thoracic chain; it also supplies sympathetic fibers to the pelvic plexus and ganglia. Anterior to the psoas muscle and fascia, posterior to the vena cava on the right but is just lateral to the aorta on the left
COMPLICATIONS: somatic nerve block of the lumbar plexus
INDICATIONS: pain that originates from the pelvis and that is unresponsive to lumbar or caudal epidural blocks. Cancer of the cervix, uterus, bladder, prostate, or rectum, also some women with chronic nonmalignant pelvic pain.
ANATOMY: postgagnlionic fibers derived from the lumbar sympathetic chain, but also visceral sensory fibers from the cervix, uterus, bladder, prostate, and rectum. Superior L5 and inferior S2-S4 (preganglionic parasympathetic fibers)
COMPLICATIONS: transient bowel and bladder dysfunction
INDICATIONS: patients with visceral or sympathetically maintained pain in the perineal area
ANATOMY: (ganglion of Walther) most caudal part of the sympathetic trunks. the two lowest pelvic sympathetic ganglia often fuse forming one ganglion in the midline just anterior to the coccyx.
COMPLICATIONS: transient bowel or bladder dysfunction
-Preganglionic sympathetic (B) fibers most sensitive
--> pain (C and A delta) --> somatosensory (A beta) fibers --> motor fibers (A alpha)
INDICATIONS: severe intractable cancer pain, can be associated with morbidity, and are not permanent (temporary destruction of nerve fibers or ganglia can be accomplished)
-ethyl alcohol causes extraction of membrane phospholipids and precipitation of lipoproteins in axons and schwann cells
-causes severe pain on injection
-preferred for celiac plexus blocks
painless, preferred for lumbar sympathetic blockade, hyperbaric
-analgesic effect that occurs at a dose lower than needed for their antidepressant action
-both actions are due to blockade of presynaptic reuptake of serotonin, norepi, or both
-older are more effective analgesics
-potentiate opioids
-differ in their S/E (antimuscarinic effects, such as dry mouth (xerostomia), impaired visual accommodation, urinary retention, and constipation; antihistaminic effects (H1 and H2), such as sedation and increased gastric pH, alpha adrenergic blockade resulting in orthostatic hypotension; and a quinidine like effect
-extensive first pass metab and are highly protein bound
-many have active metabolites
-useful in neuropathic pain, (trigeminal neuralgia and diabetic neuropathy)
-block Na gated channels
-gabapentin, phenytoin, carbamazepine, valproic acid, clonazepam
-highly protein bound and have relatively long half lives
-carbamazepine slow and unpredictable absorption so levels need to be monitored
-useful in neuropathic pain and marked agitation or psychotic symptoms
-most common agents are fluphenazine, haloperidol, chlorpromazine, and perphenazine
-can produce undesirable extrapyramidal side effects, such as mask like faces, a festinating gait, cogwheel rigidty, and bradykinesia
-long term side effects include akathisia (extreme restlessness) and tardive dyskinesia (involuntary choreoathetoid movements of the tongue, lipsmacking, truncal instability)
-hypertension, hyperglycemia, increased susceptibility to infection, peptic ulcers, osteoporosis, aseptic necrosis of the femoral head, proximal myopathy, cataracts, and rarely psychosis
(can also develop features of cushings syndrome)
-sodium retention and hypokalemia and can precipitate CHF
-treatment of conditions associated with involuntary muscle contraction (focal dystonia and spasticity).
-management of H/A and myofascial syndromes
-blocks ACh released at the synapse in motor nerve endings but not sensory nerve fibers
-improved local blood flow, relief of muscle spasms, and release of muscular compression of nerve fibers