1. The document discusses the pathophysiology of pain, which involves transduction, transmission, perception, and modulation of pain signals in the body. 2. Pain signals are transmitted from nociceptors via the peripheral nervous system to the spinal cord and brain. Various neurotransmitters are involved at different stages of transmission. 3. Pain perception is influenced by both physical and psychological factors and can be modulated in the brain using various pharmacological and non-pharmacological treatments.

1. CHAPTER 47
PAIN

2. PATHOPHYSIOLOGY OF PAIN
• Nociception involves the physiologic
mechanisms of pain processing and is divided
into:
• Transduction
• Transmission
• Perception
• Modulation

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PATHOPHYSIOLOGY OF PAIN (CONT.)

4. TRANSDUCTION
• The process of converting painful stimuli to
neuronal action potentials at the sensory level
• Nociceptors transduce noxious stimuli into
action potentials
• Chemical mediators alter the membrane
potential of the pain receptor
• Chemical mediators include K+
, H+
, lactate,
histamine, serotonin, bradykinins, and
prostaglandins
• NSAIDs prevent prostaglandin production by
inhibiting the action of cyclooxygenase

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TRANSDUCTION (CONT.)

6. TRANSMISSION
• Stimulated nociceptors transmit impulses to
the CNS by means of specialized sensory
fibers
• Primary sensory fibers include:
• Aδ: large, myelinated fibers involved in transmission
of sharp, stinging, and highly localized pain
• C: small, unmyelinated fibers involved in transmission
of dull, aching, and poorly localized pain
• Most sensory afferent pain fibers enter the
spinal cord by way of the posterior nerve
roots—travel to the substantia gelatinosa

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TRANSMISSION (CONT.)

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TRANSMISSION (CONT.)

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TRANSMISSION (CONT.)
• Many neurotransmitters and neuropeptides
involved in synaptic transmission at the spinal cord
level such as substance P, glutamate, GABA,
cholecystokinin, and calcitonin gene–related
peptide
• Pain signals transmitted by the spinal interneurons
are then conducted to the brain by ascending
spinal pathways: anterolateral tract—thalamus—
cerebral cortex—limbic system—basal ganglia

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TRANSMISSION (CONT.)

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TRANSMISSION (CONT.)
• The brain can localize a pain sensation to a
particular part of the body because nociceptor
pathways are kept in specific anatomic order in the
cord and somatosensory cortex
• Dermatomal maps are useful for locating a source
of neurologic pain

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TRANSMISSION (CONT.)

13. PERCEPTION
• Result of neural processing of pain sensations
in the brain
• Influenced by awareness, emotions, previous
experiences, and expectations
• Pain threshold—the level of pain stimulation
required to be perceived
• Pain tolerance—degree of pain an individual
is willing to bear before seeking relief
• Pain expression—the way in which the pain
experience is communicated to others

14. MODULATION
• Descending pathways from the brain to the
dorsal horn region of the spinal cord release
neurotransmitters that can inhibit synaptic
transmission of pain signals
• Opioids such as endorphins and morphine
are mediators of presynaptic inhibition
• Raphe magnus receives input from the
periaqueductal gray, which has a high
concentration of endogenous opioids, and
the rostral pons, which secretes
norepinephrine

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MODULATION (CONT.)

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MODULATION (CONT.)
• Opioids have different effects depending on the
types of receptors they activate
• Four types of opioid receptors have been identified:
mu, kappa, sigma, and delta
• Mu and kappa receptors have analgesic activities

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MODULATION (CONT.)

18. ACUTE PAIN
• Acute pain results from tissue injury and
resolves when the injury heals
• Typically accompanied by elevated heart
rate, respiratory rate, and blood pressure,
pallor, sweating, and nausea
• Short-term therapy with nonopioid and opioid
medications to provide adequate pain relief
may prevent some types of chronic pain

19. HEADACHE
• Classified according to etiologic factors
(migraine, tension, cluster, sinus)
• Migraines result from dysfunction of the
brainstem areas involved with modulation of
craniovascular afferent fibers
• Symptoms: unilateral throbbing with nausea,
vomiting, photophobia, phonophobia,
lacrimation
• Treatments: identifying and avoiding triggers,
serotonin receptor agonists, ergot alkaloids,
NSAIDs, antidepressants, and/or beta-
blockers

20. CHRONIC PAIN
• Chronic pain may be associated with a
disease process or lasts longer than the
expected healing time
• Generally not associated with signs and
symptoms of sympathetic activity
• Depression may be a significant factor for
individuals with chronic pain

21. FIBROMYALGIA SYNDROME
• Etiology unknown, but many risk factors have
been identified
• Characterized by chronic widespread pain
affecting all four extremities
• Many associated symptoms, such as sleep
disturbance/insomnia, difficulty
concentrating, fatigue, and irritable bowel
syndrome
• Treatment: restoring sleep patterns,
participating in regular exercise, and
alleviating depression
• Pregabalin is used to target pain pathways

22. CANCER-RELATED PAIN
• Associated with disease process
• May result from infiltration of organs,
compression of structures by an expanding
tumor, or as a result of cancer treatments
• Adequate pain control is a major factor
affecting quality of life

23. NEUROPATHIC PAIN
• Results from tissue injury in which the nerves
themselves become damaged or
dysfunctional
• Constant aching sensations with intermittent
sharp, shooting, burning, or shock-like pain
• Allodynia is a common finding
• May result from altered central processing of
nociceptive input
• Medications that may be most effective
include antidepressants and anticonvulsants

24. TRIGEMINAL NEURALGIA
• Sudden, momentary, but excruciating pains
along the second and third divisions of the
trigeminal nerve
• May result from compression of the trigeminal
nerve by other structures causing
demyelination and irritation
• Treatments include anticonvulsants, surgical
nerve decompression, and gamma
radiosurgery

25. DIABETIC NEUROPATHY
• Caused by damage to the large peripheral
nerves by occult inflammation and
demyelination
• Excess of smaller myelinated fibers causes loss
of inhibitory input from the spinal cord with
unopposed nociceptive afferent
bombardment
• Symptoms: numbness, tingling, weakness, loss
of vibratory tone, and proprioception
• Patient education is critical toward reducing
further complications
• Antidepressants and anticonvulsants may
help

26. POSTHERPETIC NEURALGIA
• Herpes zoster is characterized by a burning
pain that follows a dermatomal pathway and
is accompanied by a blistering rash
• Early use of antiviral medications (acyclovir or
famciclovir within 48 hours of eruption of rash)
can decrease risk of PN
• Transdermal lidocaine, capsaicin cream,
anticonvulsants, and antidepressants
commonly used to treat PN

27. ISCHEMIC PAIN
• Results from sudden or profound loss of blood
flow to the tissues
• Described as aching, burning, or tingling
• Management aimed at improving blood flow
and reducing tissue hypoxia
• Chronic ischemic pain associated with
atherosclerosis; treatment includes lifestyle
modifications: weight loss, smoking cessation,
exercise
• Surgical bypass procedures or placement of
intravascular stents may be used

28. REFERRED PAIN
• Perceived in an area other than the site of
injury
• Examples include pain of myocardial infarction
being felt in the jaw or left arm; shoulder pain after
pelvic procedures; diaphragmatic irritation from
peritonitis
• Pain is generally referred to other structures in
the same sensory dermatome

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REFERRED PAIN (CONT.)

30. PHYSIOLOGIC RESPONSES TO
PAIN
• Sympathetic nervous system activation during
acute pain can lead to:
• Increased heart rate, respirations, blood pressure
• Increased circulating blood glucose
• Decreased gastrointestinal motility
• Hypomotility of the bladder

31. PAIN IN THE YOUNG AND
ELDERLY
• Young and old often receive inadequate
pain management
• Inadequate pain treatment in neonates and
infants can result in hemodynamic instability,
catabolism, and poor surgical outcomes
• Pain perception does not decrease with
aging, but communication and expression of
pain may vary

32. TREATMENT MODALITIES
• Pain management interventions can be
directed at three points:
• Interrupting peripheral transmission of nociception
• Modulating pain transmission at the spinal cord level
• Altering the perception and integration of
nociceptive impulses in the brain

33. PHARMACOLOGIC AND
NONPHARMACOLOGIC PAIN
MANAGEMENT
• Nociceptor activation altered by
prostaglandin inhibitors (NSAIDs), heat and
cold, and local anesthetics that block sodium
influx through fast channels
• Spinal cord transmission can be altered by
cutaneous stimulation, intraspinal analgesics,
and dorsal column stimulators
• Pain can be altered by systemic opioids,
guided imagery, biofeedback, hypnosis, and
distraction

34. INTERRUPTING PERIPHERAL
TRANSMISSION OF PAIN
• Often the first step in controlling pain
• Application of heat or cryotherapy used alter
blood flow and reduce swelling
• NSAIDs decrease prostaglandins; many
significant SEs including gastrointestinal
bleeding, decreased platelet aggregation,
and renal insufficiency
• Local anesthetic agents may be used for
localized pain

35. MODULATING PAIN
TRANSMISSION AT THE SPINAL
CORD
• Cutaneous stimulation activates and recruits
large sensory fibers that can block the central
progression of nociceptive transmission at the
interneurons
• Transcutaneous electrical nerve stimulation (TENS)
• Massage
• Acupuncture
• Cryotherapy
• Therapeutic touch

36. ALTERING THE PERCEPTION
AND INTEGRATION OF PAIN
• Opioids work at specific receptor sites
located throughout the body but are highly
concentrated in the brain
• Opioid analgesics have similar mechanisms of
action but very widely in potency
• Tolerance is the need for increasing dosages to
achieve the same analgesic effect
• Dependence is characterized by withdrawal
symptoms if treatment is stopped abruptly

37. ALTERING THE PERCEPTION
AND INTEGRATION OF PAIN
(CONT.)
• Addiction is not an expected response to opioid
therapy and is a behavioral pattern of craving and
preoccupation with obtaining the drug

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ALTERING THE PERCEPTION AND
INTEGRATION OF PAIN (CONT.)