6. Tactile localization and discrimination are better when:
- Number of receptors is more.
- Receptive field is smaller.
- There is less convergence.
- Cortical area of representation is larger
8. Stereognosis
Ab Fibers Dorsal column
All types of touch receptors
Tickle & Itch
For itch: free nerve endings
For tickle: free nerve endings and Pacinian corpuscles.
C fibers Anterior spinothalamic tract
9. Proprioception
Slowly adapting receptors:
Muscle spindles in skeletal muscles.
Golgi tendon organs in tendons.
Ruffini endings in joint capsules and tissues
around the joints.
Rapidly adapting receptors:
Pacinian corpuscles in joint capsules and tissues
around the joints.
Ab Fibers Dorsal column
10. Thermal Sensation
Receptors are free nerve endings
- Few in number:
finger tips and lips > trunk.
- Moderately adapting:
Warm receptors > cold receptors
Afferents:
warm receptors send impulses along C fibers.
Cold receptors send impulses along Ad & C fibers.
Pathway:
lateral spinothalamic tract
11. PAIN SENSATION
• Unpleasant sensory & emotional experience.
• Protective sensation.
• Occurs whenever there is physical or potential tissue damage
• Causes person to react and remove the painful stimulus or seek
medical advice.
12. Pain
Receptors:
- Bare nerve terminals of Ad & C fibers.
- Slowly or non-adapting.
- most numerous in superficial layers of skin.
14. Distribution of pain receptors:
- Most numerous in superficial layers of skin.
- Numerous also in pleura, peritoneum, periosteum, joints,
wall of arteries, dura & cranial sinuses
- Less in deeper tissues.
- Few in the viscera
- Absent in liver parenchyma, lung alveoli, brain.
15. Pain sensitizers
Pain threshold
Types of Pain Sensation:
Fast pain “sharp pain”
Slow pain “dull pain”
Equal for all people
serotonin histamine
leucotrienes bradykinin
Prostaglandins K+
16. Types of Pain Sensation
According to quality of pain:
• 1- Fast (first) sharp pain:
• Aδ fibers.
• Neospinothalamic tract.
• 2- Slow (second) dull pain:
• C fibers.
• Paleospinothalamic tract.
18. C fibers
Lamina II
Substantia Gelatinosa
of Rolando SGR
Lateral
spinothalamic
tract
Reticular Formation
Paleospinothalamic
pathway
Non-specific
thalamic nuclei
Hypothalamus
All areas of
cerebral cortex
Limbic
system
Substance P
19. Perception of Pain:
Fast pain Lateral thalamus
& S I
Location &
Intensity
Slow pain Medial thalamus
& Limbic cortex
Emotional
reaction
20. Pain Perception
• Sensory cortex is not essential for
Perception of pain which occurs
subcortically in the Thalamus.
• Sensory cortex is essential for:
• 1- Localization of pain.(SSI)
• 2- Discrimination of pain modality and
intensity.(SSI)
• 3- Interpretation of its
meaning.(Association area)
• Prefrontal cortex:
contributes to accompanying
emotions and behavioral reactions.
21. Arousal Reaction:
Pain (and other sensory) input constitute part of the multisynaptic
Reticular Activating System (RAS)
3- Whole
cortex
2- Intralaminar
Thalamic N
1- Reticular
formation
22. Fast Pain Slow Pain
Occurs rapidly after stimulation Follows fast pain
Has short duration. Has long duration.
Well-localized. Poorly localized.
Arises mainly from skin, but may also arise from
peritoneum, pleura, pericardium and synovial
membranes.
Arises from skin, deep tissues and viscera.
Occurs due to stimulation of mechanical and
thermal pain receptors.
Occurs due to stimulation of all types of pain
receptors.
Carried on Ad fibers Carried on C fibers.
Chemical transmitter released at posterior horn is
glutamate.
Chemical transmitter released at posterior horn is
substance P.
Transmitted along neospinothalamic tract. Transmitted along paleospinothalamic tract.
Ends in sensory cortical areas. Ends in reticular formation, nonspecific
thalamic nuclei that project to all areas of
cerebral cortex.
Motor response is withdrawal reflex. Motor response is increased muscle tone.
Autonomic response is tachycardia and rise of
blood pressure.
Autonomic response is nausea, vomiting,
sweating, bradycardia and drop of blood
pressure.
23. Cutaneous Pain
• Definition:
• It is produced by
stimulation of pain
receptors in the skin.
• Characters:
• It occurs in two phases:
1- fast pricking (Ad)
followed by
2- Slow burning or
throbbing pain (C).
• It is accurately localized.
24. Deep Pain:
Arises from:
- muscles.
- tendons.
- ligaments.
- joints.
- periosteum and fascia.
Results from:
- mechanical trauma.
- Inflammation.
- ischemia
Example of ischemic pain is
intermittent claudication
25. 4- Ischemic Pain
• Cause:
by block of blood flow by
thrombosis, spasm or
compression.
• Due to:
accumulation of metabolites and
proteolytic enzymes
• Aggrevated by activity and
relieved by rest.
• Examples:
angina pectoris
intermittent claudication
26. Visceral pain
Causes of visceral pain:
1- Ischemia.
2- Spasm of muscle.
3- Over distention of hollow viscera.
4- Inflammation.
5- Chemical irritation.
Characters of visceral pain
1- Dull aching pain.
2- Poorly localized.
3- It is accompanied by autonomic responses.
4- It is accompanied by spasm of the overlying
muscles (guarding).
5- Usually referred to skin surface.
27. Referred Pain
• Definition:
• It is pain which is not felt in a
diseased viscus but felt on another
area away from its origin.
• Dermatomal Rule:
• Pain felt on somatic surface area
originating from same embryonic
dermatome and supplied by same
dorsal root
as the diseased viscus.
29. Mechanism of Referred Pain
1- Convergence Projection Theory
• Pain fibers from skin and
diseased viscus converge on
same SGR so will activate
same cortical neuron.
• Whatever may be the source
of pain, the cortex will project
it to skin area.
• Causes of Mis-projection:
A- brain is more accustomed.
B- skin is more exposed
C- skin is rich in pain recepors
and well represented on
cortex.
30. Mechanism of Referred Pain
2- Facilitation Theory
• Pain fibers from viscus give
subliminal fringe to nearby
SGR, receiving afferents
from skin area, increasing
its excitability.
• These neurons are now
facilitated and minor
subthreshold stimuli (light
touch) from the skin can
produce pain or
hyperalgesia.
31. Headache Referred pain
Intracranial pain-sensitive structures:
- The dura.
- Dural arteries.
- Venous sinuses.
- The tentorium.
- The brain itself is not sensitive to pain
35. Pain Control(Modulation)
• Gate Theory:
• The dorsal horn cells of spinal cord, particularly the
SGR, act as a gate for transmission of pain sensation
to the brain.
• The gate can be closed by:
• 1- Opioid Peptides.
• 2- Supraspinal Analgesia system.
• 3- Peripheral signals.
36. To the Reticular formation
Periventricular and other cortical areas
Periaqueductal
gray matter
Raphe
magnus
nucleus
Ab & Ad fibers
C fiber
Inhibitory Interneuron
Lateral
Spinothalamic tract
b-endorphin
enkephalin
serotonin
enkephalin
Substance P
SGR Gate Control
Ascending/descending analgesic system
37. Ab & Ad fibers
C fiber
Inhibitory
Interneuron
Lateral Spinothalamic tract
Substance P
SGR
Peripheral Gate control
Collaterals of Large Aβ fibers carrying tactile sensory inputs
activate inhibitory interneurons secreting GABA or enkephalin
Presynaptic inhibition of pain signals in thin Aδ or C fibers.
E.g. Rubbing, counterirritants, acupuncture.
38. Lesions of the Sensory System:
Peripheral nerve lesions:
Loss of all sensations
Gloves & Stockings in Peripheral neuropathy
Neuropathic pain e.g. trigeminal neuropathy and
phantom limb pain
39. Lesions of the Sensory System:
Tabes dorsalis
- Complication of untreated syphilis.
- Degeneration of the dorsal column and
sensory nerves in the posterior roots
Manifestations:
- Severe pain
- Loss of fine touch, pressure, vibration & proprioception.
Ataxia
40. Lesions of the Sensory System:
Syringomyelia
Pain,
Temperature
Fine touch,
pressure,
proprioception
Pain,
Temperature
43. Lesions of the Sensory System:
Fine touch,
proprioception
Pain and
temperature
Sensory effects of hemisection of the spinal cord
“Brown Sequard Syndrome”
44. Lesions of the Sensory System:
Sensory effects of thalamic lesion
Effects of lesion in somatic sensory area I
Initial loss of sensations on the opposite side
Recovery usually occurs
?? Thalamic pain
Loss of discrimination of touch, temperature and pain
45. Effects of lesion in somatic sensory association area
Patients neglect and may even
deny the contralateral side
of the body
Usually follows lesion in right parietal cortex.
Patient fails to notice or pay attention
to things or events to his left.
