2. Pain
➢A warning unpleasant sensation associated with
tissue damage
➢ Nociceptors
❑Free nerve endings,Adelta or C
❑Slowly non adapting
❑Numerous in: superficial skin layers, joints, arteries and
covering
❑Few in: viscera
❑Absent in: brain, bone, lung, liver
3. Types of Nociceptors
a.Mechanical Nociceptors (trauma/cut)
b.Thermal Nociceptors (extreme Temp)
C. Chemical Nociceptors (HCL in peptic ulcer)
d. Polymodal Nociceptors
4. Types of Pain
Ad
Fast pain
C
Slow pain
Chemical mediators of pain:
Histamine Serotonin
Substance P Bradykinin
Leukotrienes K & PGs
5. Afferent: Aδ fibers (fast pain) & C fibers (slow pain)
1st order neuron: dorsal root ganglia
2nd order neuron: posterior horn cells (same side) → cross to the
opposite side & ascend in lateral spinothalamic tract
PAIN PATHWAY
6. Lateral spinothalamic tract
2 divisions:
- neospinothalamic tract for Fast pain
- paleospinothalamic tract for Slow pain
(3rd order neuron)
PAIN PATHWAY
7. PAIN PATHWAY
Fast pain & 10 % of slow pain → specific
nuclei of thalamus → sensory cortex (SSI,II)
Thalamus
90 % of slow pain → reticular formation → nonspecific
nuclei of thalamus → whole cortex
3rd order neuron
9. Pain can be classified according to its origin:
A. Cutaneous pain
B. Deep (musculoskeletal) pain
C. Visceral (referred) pain
D. Neuropathic pain
10. Slow pain
Fast pain
Felt after fast pain
Felt rapidly
Long duration
Short duration
Poorly localized
Well localized
Arise from skin, deep tissue,
viscera
Arise from skin or covering
C → Substance P
Ad → Glutamate
1- Cutaneous Pain
11. 2- Deep Pain
Sites: muscle, tendons, ligaments, joints, fascia
Fibers: C fibers (periosteum is A delta)
Causes
• Trauma/Inflammation/Spasm/Ischemia
• Spasm: Mechanical stimulation of pain R & Compression of
blood vessels (ischemic pain)
• Ischemia → accumulation of metabolites & release of
proteolytic enzymes
e.g: Intermittent claudication
12. 3- Visceral Pain
Sites: Visceral or its Covering
➢Viscera have few pain receptors
➢Fibers: C fibers
➢Viscera COVERING are rich in
pain receptors
➢Fibers: A delta fibers
Visceral covering: pleura, pericardium, peritoneum, meninges
13. 3- Visceral Pain
Causes
• Trauma/Inflammation/Spasm/Ischemia
• Overdistention (same mechanism of spasm)
• Chemical irritation as HCL in peptic ulcer, urine
in cyctitis
14. 3. Visceral Pain
Characters:
• Dull aching, colic, over stretching
•Poor localized
• Autonomic response: hypotension, bradycardia
• Guarding of the abdominal muscles
Referred Pain: sensation at a far site in the skin
and not in the injured viscera.
15. Examples of referred pain
▪ Cardiac pain: left shoulder, arm,
root of neck, left jaw, epigastrium
▪ Gastric pain: between xyphoid &
umbilicus
▪ Gall bladder pain: mid-
epigastrium, Right shoulder, back
of tip of scapula
▪ Renal Pain: flank, inguinal
region (groin), testis
▪ Appendicitis: around umbilicus
16. HEADACHE
Intra cranial Extra cranial
Meningitis/Meningeal trauma
Brain tumors
Alcohol
Hypertension
Migraine headache
Change in intra cranial pressure
Constipation
EYE: glaucoma /Error of
refraction
Sinusitis
Toothache
Otitis media
Tension headache: spasm of neck &
scalp muscles
Referred pain
17. 4. NEUROPATHIC PAIN
Characters:
• bouts or paroxysms of electric,
burning or shooting pain
• accompanied by hyperalgesia
and/or paresthesia
Chronic pain due to damage to or pathological changes in nerve fibers.
or teeth
19. SGR act as a gate for pain transmission.
- The gate is opened by Impulses from C fibers release substance P
- The gate is closed by spinal and supraspinal inhibition:
The gate theory of pain
(1) Spinal (Peripheral) gate inhibition:
Stimulation of Aβ fibers → release of
enkephalins or GABA → inhibition of
SGR
Examples:
Rubbing or massage of skin
Counter irritation: e.g. heat
Acupuncture
(2) Supraspinal (Central) Descending
Analgesia System:
A- Hypothalamus
B- Anterior pituitary gland
C- Nuclei in the brain stem
D- Pain inhibitory area in the spinal cord
These areas secrete analgesics called
opioids → inhibition of SGR
20. Stress induced Analgesia
Soldiers wounded in the battle
Athletes wounded in the sport events
Sometimes they don’t feel pain during the stress but
experience pain later at the end.
Stress stimulates H.th or Pituitary gland to secrete
opioids
21. Lowering of pain threshold to painful stimuli.
▪ 1ry Hyperalgesia:
-Occurs in injured skin (Due to sensitization
of nociceptors)
▪ 2ry Hyperalgesia:
-Occurs in normal skin (Due to sensitization of CNS
neurons)
Hyperalgesia
The Sensory Lesions
22. 1) Mononeuropathy: loss of sensations
in the area supplied by this nerve
2) Peripheral neuropathy: in DM
Glove and stocking sensory loss
Both can also produce chronic pain called:
Neuropathic Pain
Peripheral Nerve Lesions (Neuropathy)
23. The herpes virus infects a dorsal root
ganglion
It migrates to skin → painful skin
rash and blisters (vesicles)
Herpes Zoster
24. Tabes Dorsalis
It is caused by bacteria→ neurosyphilis
Degeneration of sensory nerves in dorsal column
C/P
✓ Attacks of severe pain
✓ Loss of sensations carried on dorsal column (TOUCH,
VIBRATION, PROPIOCEPTION, STEROGNOSIS)
✓ Sensory ataxia (loss of proprioceptive sensation)
25. a) Sensory ataxia: loss of position sensation as in
tabes dorsalis or pernicious anemia which cause
destruction of posterior column
b) Cerebellar ataxia: lesion in the cerebellum
c)Vestibular ataxia: lesion in the vestibular division
of the 8th nerve.
Ataxia
Incoordination of voluntary movements without
paralysis
