Pain And Hyperalgesia Flashcards
Mention areas with NO nociceptors
Brain, bone, liver parenchyma, lung alveoli,
Describe mechanism of stimulation of nociceptors
Tissue damage leads to accumulation of pain producing substances (kinin, potassium, histamine, substance P), which stimulate chemo-sensitive pain receptors & lower the threshold for stimulation of thermosensitive and mechanosensitive pain receptors.
Higher nervous perception site of pain is ….& its adaptability is …..
Thalamus & sensory cortex
Non-adapting (tonic receptors)
Causes of cutaneous pain
Injury/inflammation of skin
Irritation of dorsal roots
Referred pain to skin other diseased deep or visceral structure
Compare fast & slow cutaneous with respect to:
1.. summation
2. Receptors
3. Perception
F, no sum, mechano-&thero-sensitive pain receptors, sensory cortex
S, sum, all esp chemo, reticular formation, specific thalamic nuclei & tectum of midbrain
Fast pain fibers terminate on ….. in spinal cord, & in ….. in thalamus
Lamina marginalis
VPLN
Slow pain fibers ends on …. In spinal cord
Lamina II & III
Enumerate structures on which Most neurons of the paleospinothalamic pathway end
- Reticular nuclei of brain stem
- Tectal area of midbrain
- Periaqueductal gray region
Causes of deep pain
- Injury/inflammation of deep structures
- Ischemia/spasm of muscles
Causes of visceral pain
- Inflammation of peritoneal covering of viscera
- Irritation/ischemia of viscera
- Spasm/overdistention of viscera
Describe characters of visceral pain
The same characters of slow cutaneous pain
May lead to: depressor autonomic effects, rigidity of overlying skeletal muscle, referred to other structures.
Compare slow & fast pain with resoect to somatic, autonomic & emotional reactions
Fast: flexor withdrawal reflex occurs, symp activity, crying, restlessless & anxiety
Slow: rigidity of overlying muscle with deep & visceral pain, para, emotional depression & sadness
2ry hyperalgesia frequently results from ……
Lesions in the spinal cord or the thalamus
Compare primary & secondary hyperalgesia
1ry: inflamed skin around injury, facilitation of pain receptors by chemicals (substance P), non-painful stimulus becomes painful.
2ry: healthy skin, convergence-facilitation theory, painful stimulus becomes more painful
CP of Zoster
Severe pain followed within few days by a rash similar to that of varicellabut is unilateral and limited in distribution to the skin innervated by a DRG
Tic douloureux is ….
Trigeminal neuralgia (5th cranial nerve)
Examples of referred pain
Gall bladder to epigastrium & tip of the rt scapula
Appendix to skin around umbilicus
Renal to skin of back, inguinal region & testis
Cardiac pain to inner aspect of left arm
Mention the dermatomal rule with examples
The pain is referred to dermatomes that share the same embryonic segment as the structure in which the pain originates.
Heart & arm has same embryonic origin, testicle migrate with supply from primitive urogenital ridge.
Compare convergence-projection & facilitation theories
P , afferents that carry visceral pain coverge on the same second order neuron that recives pain signals from the skin, the brain projects these sensations to the skin as it is always informed about it not the viscrea.
F, the afferents that carry visceral pain convege on the same spinal cord segment as the one for skin , but both have sepearate 2nd order neurons. They facilitate and even activate the nearby skin pathway.
Mention extra-cranial causes of headache
- Spasm of musckes of head & neck
- Irritation of nasal structures
- Ear disorders
- Eye disorders & errors of refraction
- Tooth disorders
Mention intracranial pain-sensitive structures
Venous sinuses, tentorium & dura at base of the brain, blood vessels of the meninges esp middle meningeal arteries.
Headache due to intracranial cause is referred to …..&…..
Frontal half of head (stimulation above tentorium)
Post part of head (occipital headache) (stimulation beneath tentorium)
List intracranial causes of headache
- Meningeal irritation
- Low CSF pressure
- Alcohol
- HTN
- Migraine (abnormal vascular phenomenon)
Describe steps of pain analgesia system in brain & spinal cord
Periventricular area of hypothalamus secretes b-endorphins which stimulate periaqueductal grey area that secretes enkephalin which stimulate magnus raphe nucleus that secrete serotonin which stimukate the pain inhibitiry complex of interneurons in the dorsal horns of the spinal cord that secrete enkephalins which cause pre & postsynaptic inhibition of pain fibers where they synapse on the dorsal horns
Mention components of brain opiate system & their sites
- B-endorphin: in hypothalamus & pituitary
- Met-&leu-enkephalin: brain stem & spinal cord
- Dynorphin: same areas as enkephalins
Explain “Gate theory”
The substantia gelatinosa is considered the gate for pain sensations. Inhibition of pain at this spinal pain gate occurs by lateral inhibition. Inhibition of pain afferents occurs by interneurons in spinal cord which release GABA or enkephalin or serotonin.
Mention sites for opioid receptors
Periventricular area of hypothalamus
Periaqueductal area
Raphe magnus nucleus
Mention sites where electrical stimulation can cause analgesia
Periaqueductal gray area, raphe magnus nucleus, periventricular nuclei, selected areas which stimulate large sensory neurons
Mention mechanisms of of surgical pain control
Cordotomy (interruption of spinothalamic pathway)
Cauterization of specific pain areas in intralaminar nuclei in the thalamus
