Somatosensory Pain and Temperature Flashcards
Properties and sensations associated with fast and slow pain.
- Fast Pain
- perceived 0.1 second after stimulus
- called sharp pain, pricking pain, acute pain
- felt in superficial, not deep tissues
- Slow Pain
- perceived>1 sec after stimulus & increases slowly over s to min
- Patient describes burning, aching, throbbing, or chronic pain.
- felt in superficial and deep tissues
- usually associated with tissue destruction
Define the terms pain, noxious stimulus and nociceptor
- Pain: “an unpleasant sensory and emotional experience associated with actual or potential tissue damage”
- noxious stimulus is one which is damaging to normal tissue.
- Nociceptors are specialized sensory receptors that are activated by noxious insult to peripheral tissue.
Types of nociceptors and their associations with afferent nerve fiber types.
- Nociceptors: free nerve endings that transduce various types of noxious stimuli into electrical activity
- Thermal Nociceptors: activated by low & high temps on the skin
- associated with Group III (Aδ) fibers
- Mechanical Nociceptors: activated by intense pressure on skin
- associated with Group III (Aδ) fibers
- Polymodal Nociceptors: activated by high intensity mechanical, thermal and/or chemical stimuli (some released by tissue damage)
- associated with Group IV (C) fibers
Transmission of noxious signals: fast pain
- Group III (Aδ) fibers (fast pain)
- thinly myelinated.
- terminate on neurons of the dorsal horn in superficial laminae.
- release glutamate, producing a fast EPSP in 2nd order neurons.
- Transmission produces depolarization peak in 2nd order neurons
- results in first (fast) pain, described as sharp or pricking
Transmission of noxious signals: slow pain
- Group IV Fibers (C-fibers) (slow pain)
- unmyelinated.
- terminate on neurons of the dorsal horn in superficial laminae.
- release both glutamate and substance P.
- Substance P enhances and prolongs the action of glutamate on second order neurons.
- Transmission produces a second, more prolonged depolarization peak in second order neurons
- corresponds to second (slow) pain, described as burning
Central Pathway of Pain
- The anterolateral spinothalamic tract is the ascending nociceptive pathway.
- The axons of relay/projection neurons in multiple lamina of the dorsal horn cross
- forms the contralateral anterolateral spinothalamic tract that terminates in the thalamus.
Neurons involved in the gate theory of pain control
-Pain transmitted along ascending spinothalamic tract gated by pathways conveying other sensory modalities.
-Neurons Involved in the Gate Theory:
*Interaction of four classes of neurons in the dorsal horn:
*unmyelinated type IV (C) primary afferent fibers for pain
*myelinated Group I&II primary afferent mechanoreceptive fibers
*projection neurons (cell bodies in multiple lamina of dorsal horn) whose axons form the ALST tract
-output determines the intensity of pain
*inhibitory interneurons: cell bodies located mainly in lamina II
axons terminate on the projection (relay) neurons
Connectivity Interaction of the Four Neurons Involved in Gate Theory of Pain Control
-Group IV (C) Fibers
*excite (+) dorsal horn projection (relay) neurons.
*Collaterals inhibit (-) firing of inhibitory interneurons in LAM II.
*If activated, pain facilitated by direct excitation of relay neurons
& inhibition of inhibitory interneuron to projection neuron of ALSTT
-Myelinated Group I and Group II Fibers
*Collaterals excite (+) inhibitory interneurons in LAM II.
*Inhibitory interneurons in LAM II inhibit activity of relay neurons of the ALSTT
-Inhibitory Interneurons (gate)
*spontaneously fire on dorsal horn relay neurons
*act to decrease the intensity of pain.
*facilitated by Group I&II (non-nociceptive, mechanoreceptor) fibers on inhibitory interneurons.
*suppressed by Group IV nociceptive fibers.
Mechanism for Opening and Closing Gate (The Gate Theory):
If only Group IV (C) fibers are stimulated to fire
- Group IV (C) fibers excite the dendrites of relay neurons.
- C fibers suppress spontaneous firing of inhibitory interneurons.
- Result in max excitation of relay neurons directly & indirectly
- max pain signals sent to ascending levels of brain by ALSTT
- “gate is open”
Mechanism for Opening and Closing Gate (The Gate Theory):
If Group I&II fibers stimulated concurrently with the C fibers
- Group I & II fibers facilitate inhibitory interneurons synapsing on dorsal horn relay neurons of ALSTT
- Results in the firing rate of ALSTT relay neurons decreasing by activating inhibitory interneurons
- fewer nociceptive signals are transmitted to ascending levels
- “gate closes”
Pain Therapies Based on the Gate Theory
- explains tendency to alleviate pain by massaging site of injury
- activates the primary mechanoreceptors of large myelinated fibers from the same dermatome.
- led to simple therapies for reducing pain:
- transcutaneous stimulation of large caliber, myelinated peripheral nerves in the region of the pain
Descending pathways can induce pain suppression.
- Some ascending spinothalamic fibers synapse in the reticular formation & the periaqueductal gray area
- Neurons of the PAG descend bilaterally
- terminate directly on serotonergic and noradrenergic neurons in the medullary reticular formation (RF).
- These RF neurons project to enkephalinergic inhibitory interneurons of LAM II of the spinal cord
- Enkephalin is thought to:
- presynaptically inhibit primary afferent pain C fiber endings
- postsynaptically inhibit projection neurons of ALSTT
Clinical Applications of Descending pathways Inducing Pain Suppression.
- Morphine acts on opiate receptors
- mimics the action of enkephalinergic inhibitory interneurons
- Descending circuits activated when strong autonomic response is generated.
- Neuropathic pain
- results from nerve injuries
- cause neurons to fire spontaneously at high rates.
- Examples:
- phantom limb: occurs in at least 90% of limb amputees and can be treated with mirror therapy
- carpal tunnel syndrome associated with injury to the median nerve at the flexor retinaculum
- usually unresponsive to opiates but respond to tricyclic anti-depressants by an unknown mechanism.
Hyperalgesia:
- increased sensitivity of nociceptors due to tissue damage
- primary hyperalgesia - at site of injury
- secondary hyperalgesia - surrounding injury site
- occurs because threshold of nociceptors decreases.
Mechanism of Hyperalgesia
- cascade of release of neuroactive peptides
- injured tissues release:
- histamine
- bradykinin
- prostaglandin
- serotonin (5HT)
- All of which sensitize the nociceptors.
- Primary afferent axon terminals in CNS release substance P
- increases the release of histamine (from mast cells)
- acts as a vasodilator to cause edema.
- Edema then causes additional release of bradykinin.
- Activity of dorsal horn superficial lamina neurons increases
- result of repetitive Group IV primary afferent fibers firing,
- contributes to the hyperalgesic state.
