Test 1 Flashcards
Algesia
Increased sensitivity to pain
Define pain
an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
Algogenic
Pain producing
Allodynia
A normally non harmful stimulus perceived as painful ie feather
Analgesia
Pain relief
Dysesthesia
An unpleasant abnormal painful sensation weather evoked or spontaneous
Hyperalgesia
Heighten pain response
Neuralgial
Painful sensation in a cluster of peripheral nerves
Neuropathy
Abnormal disturbance in the function of nerves
Paresthesia
Abnormal sensation wether evoked or spontaneous
Morphology of sharp fast pain
Myelinated A-delta (Aδ) primary afferent neurons conduct action potentials at velocities between 6 and 30 m/sec
Nocicepter
Noxious stimulus is detected by pain receptors, or nociceptors,
which are free nerve endings.
Dull achey burning throbbing pain
Smaller nonmyelinated C fibers conduct at velocities between 0.5 and 2 m/sec
mechanical, thermal, and chemical injuries
Neuropathic Pain
Neuropathic Pain caused by damage to peripheral or central neural structures resulting in abnormal processing of painful stimuli.
Often described as: 1. “burning”
2. “tingling”
3. “shock-like” etc
Somatic
Somatic Pain: pain that has an identifiable locus as a result of tissue damage causing the release of chemicals from injured cells that mediate pain.
- well localized
- sharp in nature
- generally hurts at the point or area of stimulus
Visceral
Visceral Pain: diffuse and can be referred to another area. It is often associated with distention of an organ capsule or the obstruction of a hollow viscus. Also, it is often accompanied with autonomic reflexes such as N/V/D.
- “dull”
- “cramping”
- “squeezing”
- vague in nature
Idiopathic/psych
Idiopathic or Psychogenic Pain: associated with chronic pain states and is used to describe pain that has no apparent cause. Neither nociceptive or non-nociceptive mechanisms can be identified as a cause for pain, and psychological symptoms are commonly present.
Pain transmission ascending pathway stim > brain
Spinothalamic (anterolateral) system!
1) stimulus > free nerve endings> type a delta fast or type c slow (cell bodies dorsal root ganglia of the spinal cord)
2) entering dorsal horn > tract of Lissauer
3) primary afferents enter the gray matter synapse with second-order neurons and terminate primarily in Rexed’s laminae I, II, and V.
3) Second order neurons then cross the midline of the spinal cord through the anterior commissure and ascend in the anterolateral pathway of the spinothalamic tract to the thalamus.
4) In the lateral thalamus and the intralaminar nuclei, second- order neurons synapse with third-order neurons, which then send projections to the cerebral cortex
5) perception
2 types of second order neurons
nociceptive neurons and wide dynamic range
Define wdr secondary neuron
wide-dynamic-range (WDR) neurons that receive input from both nociceptive (Aδ and C fibers) and non- nociceptive (A-β) primary afferents. WDR neurons are activated by a variety of stimulants (innocuous and noxious)
Define nociceptive secondary neuron
nociceptive (Aδ and C fibers) input
Perception
Somatosensory area of the cerebral cortex
Perception: occurs once the signal is recognized by various areas of the brain, including the amygdala, somatosensory areas of the cortex, hypothalamus, and the anterior cingulate cortex.
Define Modulation
Modulation: involves altering neural afferent activity along the pain pathway; it can suppress or enhance pain signals
occurs within the descending efferent pathways
the descending efferent modulatory pathways from the brain are
considered the body’s “analgesia system” or pain control system
Descending pathway pain perception > pain control
descending axons from the cerebral cortex, hypothalamus, thalamus, periaqueductal gray, nucleus raphe magnus, and locus coeruleus via the dorsolateral funiculis synapse with and suppress pain transmission to the brainstem and the spinal cord dorsal horn.
endogenous opioids (enkephalin/dynorphin) play an inhibitory role Pain modulation is enhanced in the presence of “Central Sensitization.”
