Pain Management 2

Front 1

1. is?
2. is?

Back 1

1. Trigger point distribution for semispinalis capitis.
2. Trigger point distribution for semispinlalis cervicis.

Front 2

1. is?
2. is?

Back 2

1. Trigger point distribution for Splenius cervicis.
2. Trigger point distribution for Splenius capitis

Front 3

Pictured?

Back 3

Trigger point distribution/referral pattern for Trapezius

Front 4

Pictured?

Back 4

Trigger point referral pattern for Levator scapulae.

Front 5

What is pictured? When would this occur?

Back 5

Neurogenic Inflammation:
Activated microglia release several pro-inflammatory cytokines, chemokines, and other agents that modulate pain processing by affecting either presynaptic release of neurotransmitters and/or post-synaptic excitability

Would occur post peripheral nerve injury.

Front 6

Examples of this type of pain are ACNES, meralgia, paresthetica, compressions (EtOH, cancer)

Back 6

Peripheral neuropathic pain

Front 7

Activated microglia release several pro-inflammatory cytokines, chemokines, and other agents that modulate pain processing by affecting either presynaptic release of neurotransmitters and/or post-synaptic excitability

Back 7

Neurogenic inflammation (post-peripheral nerve injury)

Front 8

What are the mechanisms of neuropathic pain?

Back 8

• Spontaneous discharges or disregulated discharges
• Abnormal expression of ion channels
• Localized demyelination
• Disregulated cell bodies in DRG
***Each mechanism provides a different Tx approach***

Front 9

This is an example of what type of pain:
Right shoulder pain post larparoscopic surgery (due to a sub-phrenic gas bubble)

Back 9

• Somatic-somatic
Diaphragm is a muscle - not hollow ∴ a somatic structure

Front 10

Visceral afferent nociceptors and afferent pain-projection neurons from a somatic structure synapse on the same neuron in the DRG. The brain projects the visceral sensation onto the somatic structure. This is the definition of?

Back 10

Convergence-Projection Hypothesis.

Front 11

What is the convergence-projection hypothesis?

Back 11

• Visceral afferent nociceptors converge on the same pain projection neurons as the afferents from the somatic structures in which the pain is perceived. The brain projects the sensation on to the somatic structure.
• AKA referred pain

Front 12

Brain Freeze (cold stimulus on the vagus giving a headache) is an example of?

Back 12

Referred pain (Convergence-Projection Hypothesis in action)

Front 13

The thoracic parietal pleura, periphery of the diaphragmatic pleura, & upper 85% of the abdominal wall are all supplied by ____? Which means?

Back 13

• All supplied by T6 & T7.
• This means that pain from any of these structures can feel the same.

Front 14

I'm used to the pain

Back 14

Habituation

Front 15

I have a lower pain threshold than before the accident

Back 15

Sensitization

Front 16

Intense, repeated, or prolonged stimuli applied to damaged or inflamed tissues reuslts in a ↓ of the threshold for activating 1º afferent nociceptors, and an ↑ in the frequency of firing for all stimuls intensities.

Back 16

Neurogenic inflammation (Sensitization in the periphery)

Front 17

_____ likely has a role in the pathogenesis of asthma, fibromyalgia, eczema, migraines, rosacea, dystonia, & psoriasis.

Back 17

Neurogenic inflammation

Front 18

Inflammatory mediators such as bradykinin, nerve growth factor, some prostaglandins, and leukotrienes contribute to this process ______. Silent nociceptors may also be involved.

Back 18

Neurogenic inflammation

Front 19

1. Pressure causes cell damage, ↓ pH, release of K+, syntehsis of prostaglandins & bradykinin, ↑ sensitivity to BK & other pain substances.
2. The Peripheral afferent nociceptor signals the spinal cord, but also induces the release of peptices that cause vasodilation and neurogenic edema (bogginess), w/ release of histamine from mast cells and serotonin from platelets.

Back 19

Neurogenic inflammation

Front 20

If a mechanical stimulation (heel jar) causes abdominal pain, what can be inferred?

Back 20

There is sensitization (the abdominal organs are sitting in an inflammatory soup caused by neurogenic inflammation)

Front 21

What can be used to tx neurogenic inflammation?

Back 21

• OMM - mobilizes extracellular fluid
• Botox

Front 22

An intiial noxious event causes centra hyperexcitation w/in the dorsal horn cells, w/ upregualtion of the pain response from further noxious stim.

Back 22

Central Sensitization

Front 23

1. Expansion of the receptive fields
2. Short term "wind-up"
3. Long term "amplification

Back 23

Central Sensitization

Front 24

A, B, and C fibers have their cell bodies in the DRG. They sometimes respond to stim from receptor fields that are much wider than a single dermatome (so exam findings may deviate from expected dermatomal outlines). This is an example of?

Back 24

• Expanding receptive fields (part of Central Sensitization)

Front 25

What two neurotransmitters are used by inhibitory neurons?
What two NT are used by excitatory neurons?

Back 25

• GABA or glycine
• Glutamate and aspartate

Front 26

How is GABA synthesized?

Back 26

GABA is synthesized from glutamate by glutamate decarboxylase which uses pyridoxal phosphate (B6)

Front 27

Mediated by NT in and neurotrophic factors such as: glutamate, sub. P, neurokinins, calcitonin gene-related peptige G-protein coupled receptors, ligand gated ion channels, Trk receptors, NO, and prostanoids
• Glutamate excites wide-dynamic range neurons. The more they fire, the lower the threshold of the C fibers --> less input generates more pain
ª Opioid and glutamate-R antatgonists (tramadol, methadone, dextromethorphan), can help prevent this effect.

Back 27

Wind-up (part of Central Sensitization)

Front 28

What drugs are useful for preventing wind-up? Why?

Back 28

• Tramadol, methadone, dextromethorphan
• They are opioids and glutamate-R antagonists

Front 29

Regulatory interneurons wind down, w/ less inhiitory messaging.
• Vg-Ca++ channel blockers, NMDA-R antagonists, NO syntease inhibitors, and agents that increase inhibition can block this ___.
• This can also be worsened by what?

Back 29

Amplification (part of Central Sensitization)
• Sympathetically maintained activity can generate loss of inhibitor effect of GABA

Front 30

What drugs are effective against amplification? Why?

Back 30

• Gabapentin
• Pregabalin
• They are Vg-C++ channel blockers

Front 31

Stimulation of large afferents activate the release of inhibitory glycine (rubbing vigorously on the area of an injury. This is ______?

Back 31

• Gate Control theory

Front 32

Electircal stim devices which stimulate fine-diameter interneurons are employing what method of pain modulation?

Back 32

• Gate Control theory

Front 33

• Inflammatory signaling molecules trigger Na+ channel phosphorylation
• Gene transcription altered at the DRG and dorsal horn neurons
• Lower activation threshold and larger current when activated

Back 33

Peripheral sensitization (a Neuropathic pain mechanism)

Front 34

• Peripheral nociceptor inpts trigger molecular ∆s in central neruons
• Less GABA and glycine inhibition
• More MNDA and AMPA activation
• Death of inhibitor interneurons

Back 34

Central senstization (a Neuropathic pain mechanism)

Front 35

• Constant activation of the polymodal (wide dynamic range) fibers w/ ongoing release of neuropeptides (sub. P, calcitonin-gene-related peptide) causing ongoing neurogenic inflammation in the periphery, central wind up
• What drugs help here?

Back 35

• Persistent inflammatory pain model
• NSAIDs are effective here

Front 36

• Collateral sprouting after peripheral nerve injury and axonal degeneration w/ ectopic discharges
• What drugs help here?

Back 36

• Persistent neuropathic pain model
• Local anesthetics effective here

Front 37

• Loss of inhibtory fxn of GABAergic dorsal cells leads to excessive glutamate/aspartate
• What drugs help here?

Back 37

• Persistent neuropathic pain model
• Anti-epileptic drugs help here.

Front 38

Spontaneous pain & sympathetic dysfxn following injury

Back 38

Complex Regional Pain syndrome

Front 39

Spontaneous pain & sympathetic dysfxn following injury + identifiable nerve injury

Back 39

Complex Regional Pain syndrome I (or Post-traumatic neuralgia)

Front 40

Spontaneous pain & sympathetic dysfxn following injury + NO identifiable nerve injury

Back 40

Complex Regional Pain syndrome II (Reflex sympathetic dystrophy)

Front 41

What potentially catastrophic ddxs should come to mind w/r/t pain?

Back 41

• Cancer
• Infection
• Fractue
• Ongoing tissue damage (nerve compression)

Front 42

Lumbalgia + Hx of longstanding steroid use = possible ____

Back 42

Osteoporotic fracture

Front 43

Lumbalgia + unexplained fracture = ______

Back 43

Malignant involvement of the bone

Front 44

Pelvic pain + increasing abdominal girth = possible ____

Back 44

Ovarian cancer

Front 45

What are some red flags w/r/t pain?

Back 45

• Children, age > 5.
• Fevers, chills, night sweats, penetrating wound
• Unrelenting night pain or pain at rest
• Progressive motor/sensory deficit
• Unexplained distribution
* Unexplained weight loss
• Hx of cancer
• Hx of steroid use, immunosuppression, IV drug use
• Failure to improve after 6 wks conservative Tx.

Front 46

Depression occurs in up to ___ of chronic pain pts. Anxiety in ____ of chronic pain patients. What other psych things may be seen?

Back 46

• 80%
• 30%
• Substance abuse and PTSD often seen.

Front 47

What are Waddell's signs?

Back 47

• Help to determine if a patient is faking their pain.

Front 48

A stellate ganglion block often terminates this kind of pain

Back 48

Sympathetically mediated pain

Front 49

Peripheral nerve damage without autonomic change (post-herpetic neuralgia, neuroma formation) is referred to as ___ type of pain.

Back 49

Non-sympathetically mediated.

Front 50

• disturbance of function or pathologic changes in a nerve. vs.
• disturbance of function or pathologic changes in one or more nerve roots.

Back 50

• Neuropathy vs. Radiculopathy

Front 51

Term for undertreating pain.

Back 51

Oligoanalgesia

Front 52

Polymyositis, dermatomyositis, polymyalgia rhematica, spacticity, & thalamic pain are all examples of _____

Leavator ani syndrome, Proctalgia guhax, DeQuervain, Meralgia paresthetica, & Burning mouth syndrome are all examples of _________

Back 52

Generalized Chronic Pain syndromes
(also includes Fibromyalgia & Sickle Cell)

Localized Chronic Pain syndromes

Front 53

• Mild pain: non-opiod +/- adjuvant
• Moderate pain: opioid and non opioid +/- adjuvant
• Severe pain: opioid +/- adjuvant, and non-opioid

The above describes

Back 53

Analgesic stepladder

Front 54

Lidoderm/EMLA and Capsaicin are examples of?

Back 54

Topical analgesics

Front 55

Examples of these type of pain-management drugs are: sodium channel blockers (Anticonvulsants and antiarrhythmics), mood stabilizers, antidepressants, muscle relaxers, marijuana, antihistamines

Back 55

Co-analgesics

Front 56

What co-analgesic is especially useful for neuropathic pain?

Back 56

Anti-convulsants

Front 57

Carbamazepine, gabapenting, pregabalin, phenytoin & vaproic acid are often used as co-analgesics for what type of pain?

Back 57

Neuropathic pain

Front 58

How are TCAs useful as co-analgesics? SNRIs?

Back 58

• TCAs inhibit Na+ channels and block NMDA receptors
• SNRIs inhibit the reuptaek of biogenic amines (NEP, 5-HT) ↑ [ ] & duration of action at the synapse

Front 59

What co-analgesics are useful for chronic pain and MS?

Back 59

Antispastics (skeletal muscle relaxants) Baclofen & dantrolene

Front 60

What co-analgesics are usefulf for musculoskeletal conditions?

Back 60

Atispasmodics (skeletal muscle relaxants) Carisoprodol, cyclobenzaprine, metaxalone, methocarbamol.

Front 61

Prazoin, terazosin, phenoxyenzamine (are ___?) and clonidine ( ___?) are used for what?

Back 61

• Prazosin, terazosin, phenoxybenzamine are all alpha-1 antagonists
• Clonidine (alpha-2 agonists)
• All used as sympathetic nervous system blockers

Front 62

Helpful for opioid-induced nausea, and especially useful because it potentiates the analgesic effects, possibly by blocking histamine mediated activation of C fibers.

Back 62

Hydroxyzine

Front 63

What drug inhibits release of NEP from the postganglionic adrenergic neurons, producing a chemical sympathectomy?

Back 63

Lidocaine

Front 64

Babes exposed to opioids close to delivery may have ____

Back 64

Respiratory depression

Front 65

Babes exposed to COT during pregnancy may ___

Back 65

WILL go through excrutiating w/drawal

Front 66

Babes exposed to NSAIDS late in pregnancy may have ____

Back 66

Constriction of the ductus arteriosus

Front 67

What are some key side-effects of NSAIDs?

Back 67

• GI upset, gastritis, upper GI bleed
• Elevated BP
• Derm RXNs
• Exacerbation of bronchospasms
• Nephrotoxicity

Front 68

What are some of the risk factors to consider when prescribing opiods?

Back 68

• Age < 45, ♀, family Hx of abuse, smoker
• Psych: substance abuse, Hx of sexual abuse, major psych ddx
• Social: legal probs, MVAs, poor support

Front 69

What should be included in the medication contract/policy agreement?

Back 69

• Definiition of Tx goals
• Informed consent
• Clinic policies and procedures
• Exit strategy

Front 70

What are the four A's? What are they used for?

Back 70

• Analgesia
• Adverse effects
• Activities of daily living
• Aberrant behaviors

Used during Chronic Opioid Therapy

Front 71

Primary chronic neurobiological disease with genetic, psychosocial, and environmental factors influencing its manifestation.

Back 71

• Addiction
• Continued use despite harm

Front 72

What can help allay the nausea and vomiting sometimes caused by opioids?

Back 72

• Antidopaminergic, antiserotonergics, anticholinergics

Front 73

What opiod can cause a prolonged QT?

Back 73

Methdone

Front 74

Classic neuropathic pain (intense burning pain, hyperalgesia, allodynia)
• Autonomic features (altered sweating, skin color, skin temp)
• Trophic changes to skin, hair, nails
• Altered motor function (loss of strength, decreased ROM, tremor

Back 74

Chronic Regional Pain Syndrome (CRPS)

Front 75

How will the skin around an area of CRPS appear?

Back 75

• ↑ sweating, heat, hair growth