Pain Mgt_Exam I

cell bodies of first order neurons is in the dorsal root ganglia, with its axons extending to periphery

the greater the impulse of a stimulus, the greater the frequency of impulse firing

• specialized thermoreceptors
• mechanoreceptors
• chemoreceptors
• polymodal receptors
• unspecialized meissner's and Pacinian corpuscles

Alogens: bradykinin, histamine, serotonin, 5-HT, Hydrogen, Potassium, prostaglandins, capsaicin

Stimuli: mechanical, chemical, thermal

—Psych eval for pain useful when Medical evaluation fails to reveal cause of pain, or Pain intensity is disproportionate to disease or injury

• —Test used to define role of psychological or behavioral role in pain
• —-Minnesota Multiphase Personality Inventory (MMPI)
• -Back Depression Inventory

• —Pain can cause emotional disorders and vice versa
• —-Difficult to determine which came first (Chicken or the EGG)
• -Important to treat BOTH the pain and the emotional stress

• —EMG & nerve conduction studies are useful for dx of
• -Entrapment syndromes
• -—Radicular syndromes
• -—Neural trauma
• -Polyneuropathies

—Diagnostic neural blockade: uses LA to specify a pain mechanism

• By Duration-
• Transient Acute Pain
• Chronic Pain

• —By Etiology-
• —Nociceptive
• —Inflammatory
• —Neuropathic

• —By Severity-
• —Mild
• —Moderate
• —Severe

• —By Anatomy-
• —Somatic
• —Nociceptive,
• —Of skin, SC tissue, bone, muscle
• —Well localized

• —Visceral
• —Nociceptive,
• —Of internal organs,
• —Poorly localized

• —Referred
• —Perceived as occurring in an area other than the stimulus

• Acute pain has a protective biological fcn (eg p/o pain)
• - short term lasting up to 6 mo

• Acute pain is r/t Nociceptive transmission (somatic/visceral)
• - major NT is Glutamate

assoc/psych s/sx are minimal

Transmitted via normal pathways Originating by stimulation of nociceptors

• —Transmitted via Ad (first pain) or C fibers (second
• pain)

Either somatic or visceral

• —Pain consists of four processes:
• —Nociception (depolarization at the peripheral nociceptors)
• —Transmission (along primary afferent nociceptive axons to the SC --> to the brain)
• —Perception (intellectually recognized by the brain as pain)
• —Modulation (augmentation or inhibition at multiple levels)

—Phase II Pain

—Serves no protective biological function

—Persist beyond expectations (>3-6 months)

—More intense than stimulus warrants (sensitization)

—Can be either nociceptive or neuropathic

—The major neurotransmitter of chronic pain is Substance P (also glutamate and aspartate)

chronic pain is rarely treated effectively

• The dorsal horn has been bombarded by severe pain for a long period of time
• -The interneuron adjusts by adding fast pain receptors to amplify pain signal--> to the ascending tract --> brain recognizes severe intractible pain --> modifier pathways attempt to inhibit pain but fails

—Precipitated by an insult to the integrity of tissues at a cellular level.

• —Endogenous susbstances can sensitize nociceptors: the inflammatory "soup"
• —Mast cells release histamines and 5HT
• —Macrophages activate fibroblasts, which in turn release IL and TNF
• —Cyclooxygenase activates prostaglandin and leukotrienes
• —The hyperemia associated with inflammation delivers NO and bradykinin

—Inflammatory mediators can directly affect nociceptors or may sensitize them to touch or movement, even some distance from the inflammatory field

• A-Beta nerve fibers
• - these nerve fibers pass through the highly sensitized cells in the dorsal horn--> SC --> transmitted as pain
• --------
• —If this increased pain lasts it can cause wind up pain in the cell bodies of the dorsal horn interneurons and further induce wide dynamic range neurons to stimulate sympathetic coupling

• Neuropathic pain, phase III pain PATHOGENIC
• —Produced by pathologic changes or damage to
• —-Peripheral nerves
• —-Central nerves

• —Can result from
• —-Partial of complete nerve transection
• -Nerve compression
• -Infectious etiology
• -—Inflammatory etiology
• -—Ischemic etiology

• Pain response is exaggerated and can be
• -—Spontaneous
• -—Evoked by innocuous stimuli

• —Described as
• —-Burning
• -Electric
• -Tingling
• -—Shooting

• —The hallmarks of neuropathic pain are
• —Allodynia
• —Hyperalgesia

• - Diabetes (others: Amputation, chemo, HIV/MS, spine sx)
• ----------
• —deafferentation within the peripheral nervous system
• — neuropathy

• —deafferentation within the central nervous system
• — post–thalamic stroke

• —an imbalance between the two
• — phantom limb pain

C-fiber nociceptors develop adrenergic receptors --> synpathetically maintained pain

...connections connections between sensory and sympathetic fibers, and such cross–connections may play a role in the pathogenesis of sympathetically mediated pain

sensitization of neurons can occur within the dorsal horn

—After peripheral nerve injury, these large afferents gain access to spinal regions involved in transmitting high intensity, noxious signals, instead of merely encoding low threshold information

• long–term potentiation (LTP), which involves a long lasting increase in the efficacy of synaptic transmission.
• Where "wind–up" is thought to last only minutes, LTP lasts at least one hour and maybe even months. Both "wind–up" and LTP are believed to be part of the sensitization process involved in many chronic
• pain states
• -----------

• —NMDA-type glutamate receptors are formed when the dorsal
• horn is bombarded with pain for an extended period of time.

• —NMDA receptor
• activation triggers a cascade of events leading to sensitization of dorsal horn
• wide dynamic range neurons

• —The NMDA receptor
• antagonists ketamine and dextromethorphan can block this cascade of events
• which contribute to sensitization

• Thalamic Pain Syndrome (Dejerine Roussy Syndrome), Posterior Thalamic Syndrome, Retrolenticular Syndrome, Central Post-Stroke Syndrome
• ------
• there is damage to sensory nerve cells in the central nervous system anywhere from the thalamus down through the spinal cord, usually the spinothalamic tract
• ------
• SCI (incidence is 7.5% to 40% to 69%)

—Stroke (generally involving the thalamus, incidence is ~ 1 in 1500)

—Multiple sclerosis

• —Cancer (when it damages CNS sensory nerve cells or the
• thalamus)

• —Physical trauma (such as surgery, gunshot, falls, MVAs,
• etc.)

Any condition that causes nerve demyelination or other nerve or brain damage

• —The Triad:
• Burning pain, often with a paradoxical component of cold, made worse by light touch or the rubbing of clothing.
• ----------

• —Symptoms: "the worst pain known to man."
• steady, deep burning, aching, cutting, tearing sensation, mixed with sudden, excruciating shots of pain, often mixed
• with other distracting sensations like cold, tingling, a "pins and needles" effect, a ballooning sensation, throbbing, and the feeling of a dental probe on a raw nerve. Intense
• skin reactions such as burning, stretching, tightness, itching, or a crawling feeling that can be irritated by any light touch
• ------
• No definitive tx

—Radiculitis is pain "radiated" along the dermatome of a nerve

—A radiculopath is caused by compression, inflammation and/or injury to a spinal nerve root

• —Examples:
• —Sciatica
• —Some lower back pain
• —Cervical radiculopathy

—meaning "other pain", is an exaggerated painful response to normally non-noxious non-painful stimuli

• —Mechanical/Tactile allodynia
• —Pain from light touch/pressure applied to the skin in the
• area of the damaged nerve

• —Thermal allodynia
• —Pain from normally mild skin temperatures in the affected
• area
• ----------
• the associated nerve damage results in decreased firing thresholds of nociceptive fibers

peripheral nerve injury could induce collateral sprouting of non-nociceptive primary afferent neurons, such as A-beta low threshold mechanoreceptors, into the superficial (nociceptive) lamina in the dorsal horn of the spinal cord

An increased response to a stimulus that is normally painful or noxious

• Caused by increased excitability of central and
• peripheral nociceptive neurons caused by tissue
• injury

• —Primary hyperalgesia
• —-found in the immediate area of tissue injury and is
• caused by sensitization of local primary afferent nociceptors by inflammatory mediators

• —Secondary hyperalgesia
• —-develops around and beyond the immediate area of injury: this is centrally mediated, influenced by a number of receptor systems at the spinal level