CH.6: Pain

Epidemiology of Pain

• protective mechanism

• MOST COMMON SYMPTOM for which people seek treatment for

• Pain management is important because it speeds up rate of recovery and you have fewer post-op complications

Pain Ascending Signals

Nociceptors: pain receptors

• A-delta fibers: large and myelinated (fast conduction) EX: pulling hand away from something hot

• C fibers: small and unmyelinated (slow conduction) EX: pain after the burn has taken place

Spinothalamic tract: carries pain signals to the brain; crosses over right when sensory fibers reach spinal cord

Brain: perception of pain

Pain Descending Signals

Brain: Interprets pain sensory signal and sends outgoing signal through the corticospinal tract

Endogenous opioids: natural analgesic neurochemicals that blunt/modify pain signal EX: endorphins, enkephalins, dynorphins

Receptors on pain fibers: opioids bind to receptors and block pain signals

Brain vs Neurotransmitter Role

Brain: SENDS outgoing signals to modify pain (control center)

• manufactures and releases endorphins

Neurotransmitter: excite/inhibit pain signals (what pain meds try to modify)

Simple Reflex Arc

Protective responses that DO NOT involve the brain

EX: Patellar reflex

• Afferent neuron: (sensory) receives signal and sends to dorsal horn of spinal cord

• Interneuron: (integration) connects sensory neuron to spinal motor neurons

• Efferent neuron: (motor) receives outgoing signal from spinal cord

ALL WITHOUT GOING TO THE BRAIN

Neurotransmitters and Pain

Prostaglandins: enhance inflammation, pain, edema

Interleukins: enhance inflammation, pain, edema

Tumor necrosis factor: enhance inflammation, pain, edema. decreases appetite

Leukotrienes: enhance inflammation, edema, bronchospasm (asthma, allergy)

Bradykinins: enhance inflammation

Glutamate: amplifies pain signal

Substance P: amplifies pain signal

Enkephalins, endorphins: inhibitory influence on pain, natural opioid

Acetylcholine: inhibitory influence on pain in the spinal cord

Gamma-aminobutyric acid: inhibitory influence on pain in the spinal cord and brain

Norepinephrine: inhibitory influence on pain in the spinal cord

Dopamine: inhibitory influence on pain in the spinal cord and the brain

Serotonin: conveys analgesic signals from PAG area to the NRM area of brain (serotonin diminished in migraine heachache)

Gate Control Pain Theory

1. Transduction: “Something happened!” pain receptors notice stimuli

2. Transmission: “Let’s send a message” pain travels to spinal cord

3. Modulation: “Red light/Green light?”

• open gate: interneuron sends signal up spinal cord to the brain

• closed gate: interneuron blocks signal to the brain

  • EX: long distance runners may be in physical pain but their neurotransmitters dampen it

4. Perception: “Ouch!” conscious awareness of pain

AKA: Injury → nerves → spinal cord(turn pain up or down) → brain

Explains how pain signals travel to and from brain, how pain is not necessarily proportional to the injury BUT not phantom limb pain

Neuromatrix Theory of Pain

Pain is a multidimensional experience and is generated from a dataset of all the experience a person has throughout their life

EX: phantom limb pain - brain has built in '“pain map” so it may continue to produce sensations

Types of Pain

Acute: lasts hours/days but resolves

Chronic: beyond expected length that does not serve a biological/protective function; over 6 months

• may profoundly affect quality of life

Neuropathic: injury or malfunction of nervous tissue; burning, tingling, paresthesia (pins and needles)

Sensitization of Pain

Triggered genetics/diseases exaggerates excitement of pain nerve fibers and decreases pain inhibitory signals

EX: someone’s 2/10 pain is another’s 10/10 pain

SOURCES OF PAIN

• Cutaneous: well-defined (localized) and short lasting; but you feel it more because it’s just below the skin where there are many nerve endings

  • EX: minor cuts and burns

• Deep somatic: dull, poorly localized pain, longer lasting

  • EX: ligament, tendon, blood vessels, nerves

• Visceral: vague, not localized, from distended hollow organs

  • EX: deep organs

• Referred: pain occurs at distance from actual pathology

  • EX: myocardial infarction - nerve fibers from region of high sensory input + nerve fibers from region of low sensory input converge on same level of spinal cord so even if it’s near the chest, you feel pain on your left arm

• Phantom: amputated part of body

Dermatomes and Myotomes

Dermatomes: skin area innervated by sensory fibers of single nerve root

Myotomes: group of muscles innervated by motor fibers of single nerve root

where the symptoms are helps us identify which spinal nerve is affected

EX: sciatica is nerve pain from impingement between L4-S1

Pain Assessment

Considered the 5th vital sign

SUBJECTIVE

CULTURE has a strong impact on reporting pain

Distinguishing features of pain can help diagnose it

EX: Murphy’s sign in cholecystitis

OLDCART Pain Assessment

O: when did the pain begin?

L: where does it hurt?

D: how long does it last?

C: what does it feel like?

A: does anything make it worse?

R: does anything make it better?

T: did anything make it better? (meds, ice, heat)

Pain Assessment Scales

1. Numeric Rating: 1-10

2. FLACC: Face Legs Activity Cry Consolability (infants, children)

3. Wong-Baker Faces

4. PAINAD for dementia patients

Treatment for Pain

When using pain meds, each should have a diffierent mode of action

1. Mild pain: nonopioid analgesics, NSAIDs

2. Moderate pain: weak opioids

3. Severe pain: strong opioids

4. Acute, chronic, palliative: adaptation, rehab for comfort

NSAID with or without adjuvant for each step

Pharmacological Pain Relievers: Opioids

Controlled substance

EX: morphine - produces analgesia, euphoria, sedation

Most effective when given before onset of pain

Can cause constipation, nausea, dizziness, dependence, addiction

Pharmacological Pain Relievers: Nonopioid Analgesics

Acetaminophen (Tylenol) - reduce pain, fever but NOT inflammation

NSAIDs (relieve pain, fever, edema, inflammation) - aspirin, ibuprofen, naproxen, celecoxib

• blocks prostaglandin (messengers of pain) synthesis by inhibiting COX enzymes

  • COX-1 (good stuff): protects stomach lining, maintain blood flow, helps with clotting

    • NSAIDs can inhibit this and COX-2

  • COX-2: causes inflammation and pain

    • celecoxib inhibits just this enzyme

Most NSAIDs block COX-1 and COX-2 meaning they block the good stuff AND the pain, so you can heave increased GI problems, kidney problems, increased bleeding

Pharmacological Pain Relievers: Adjuvant Medications

Not habit forming

Amplify analgesic effects of pain medication: antidepressants, local anesthetics, anticonvulsants (Gabapentin for nerve pain) cannabinoids, topical pain relievers

EX: Percocet = oxycodone (analgesic) + acetaminophen

Nonpharmacological Pain Management

• physiotherapy

• OT

• Acupuncture

• TENS

• virtual reality

• botox

• Psychological counseling

Cancer Pain

Cannabis use

Intermittent or chronic pain

Tumors can cause pain by placing pressure on adjacent structures

Chemotherapy and radiation therapy can cause inflammation and tissue destruction

Spinal Nerve Radiculopathy

Spinal nerve impingement

Lumbosacral area

Affects sciatic nerve with pain radiating down leg with numbness and tingling (sciatica)

Cervical radiculopathy: spinal nerve impingement in neck area leads to numbness in hand and fingers

Diabetic Peripheral Neuropathy

Compromised blood flow and circulation

Both sensory and motor nerves are affected

• high glucose levels cause cellular damage and nerves break down

Loss of pain sensation may cause pt to be unaware of wounds on the feet

Postherpetic Neuralgia

“Chickenpox”

Remains dormant along nerves but can re-emerge as "shingles”

Produces acute, vesicular, linear rash along specific nerve; painful paresthesia

Airborne precautions before and after onset of vesicular lesions

Fibromyalgia

Pain in specific, exact tender points

Diagnosis must involve pain in 11/18 tender sites

More common in women, joints unaffected

Post-operative Pain

Meds can be used preoperatively or during surgery

Pharmacological and nonpharmacological modes of analgesia