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Part 3
Sensory Function of the Nervous
System
I Sensory pathways
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Sensory systems allow us to detect, analyze and
respond to our environment
“ascending pathways”
Carry information from sensory receptors to the
brain
Conscious: reach cerebral cortex
Unconscious: do not reach cerebral cortex
Sensations from body reach the opposite side of
the brain
1. Sensory receptors
A: Free nerve endings (pain, temperature)
A
B: Pacinian corpuscle (pressure)
C: Meissner’s corpuscle (touch)
B
C
D: Muscle spindle (stretch)
D
Ruffini's endings respond to tension and stretch in the skin
2. Sensory pathways: 3
neurons
 1st:
enters spinal cord from periphery
 2nd:
crosses over (decussates), ascends
in spinal cord to thalamus
 3rd:
projects to somatosensory cortex
2.1 Spinothalamic pathway
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Carries pain, temperature,
touch and pressure signals
 1st neuron enters spinal
cord through dorsal root
 2nd neuron crosses over in
spinal cord; ascends to
thalamus
 3rd neuron projects from
thalamus to somatosensory
cortex
spinothalamic
pathway
Spinothalamic Pathway
Primary somatosensory
cortex (S1)
Thalamus
Medulla
Small sensory fibres:
Spinothalamic
tract
Spinal cord
Pain, temperature,
some touch
Spinothalamic damage
spinothalamic pathway
Left
spinal cord injury
Loss of sense of:
•Touch
•Pain
•Warmth/cold
in right leg
2.2 Dorsal column pathway
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Carries fine touch, vibration
and conscious proprioception
signals
 1st neuron enters spinal cord
through dorsal root; ascends
to medulla (brain stem)
 2nd neuron crosses over in
medulla; ascends to thalamus
 3rd neuron projects to
somatosensory cortex
Two-Point Discrimination
dorsal
cloumn
pathway
Dorsal column pathway
Primary somatosensory
cortex (S1) in parietal
lobe
Dorsal column
nuclei
Thalamus
Medulla
Dorsal column
Medial
lemniscus
Spinal cord
Large sensory nerves:
Touch, vibration, two-point
discrimination, proprioception
Dorsal
column
damage
dorsal column
pathway
Left
spinal cord injury
Loss of sense of:
•touch
•proprioception
•vibration
in left leg
Dorsal column damage
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Sensory ataxia
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Patient staggers; cannot
perceive position or
movement of legs
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Visual clues help movement
Central
Pathways
3.3 Spinocerebellar pathway
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Carries unconscious
proprioception signals
Receptors in muscles &
joints
1st neuron: enters spinal
cord through dorsal root
2nd neuron: ascends to
cerebellum
No 3rd neuron to cortex,
hence unconscious
Spinocerebellar tract damage
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Cerebellar ataxia
 Clumsy movements
 Incoordination of the limbs (intention
tremor)
 Wide-based, reeling gait (ataxia)
 Alcoholic intoxication produces similar
effects!
4. Somatosensory cortex
Located in the postcentral gyrus of the
human cerebral cortex.
Spatial orientation of signals.
1) Each side of
the cortex
receives
sensory
information
exclusively
from the
opposite side of
the body
(the exception:
the same side
of the face).
2)The lips, face
and thumb are
represented by
large areas in the
somatic cortex,
Spatial orientation of signals.
whereas the trunk
and lower part of
the body, relatively
small area.
3)The head in the most lateral portion, and the
lower body is presented medially
II . Pain
“Pain is an unpleasant sensory and emotional
experience associated with actual or
potential tissue damage or described in
terms of such damage”
International Association for the Study of Pain
Why feel pain?
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Gives conscious awareness of tissue
damage
 Protection:
– Remove body from danger
– Promote healing by preventing further damage
– Avoid noxious stimuli
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Elicits behavioural and emotional responses
1. Nociceptors
free nerve endings in
skin respond to
noxious stimuli
Nociceptors
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Nociceptors are special receptors that respond only
to noxious stimuli and generate nerve impulses
which the brain interprets as "pain".
Nociopectors
Adequate Stimulation
–Temperature
–Mechanical damage
–Chemicals (released from
damaged tissue)
Bradykinin, serotonin,
histamine, K+, acids,
acetylcholine, and proteolytic
enzymes can excite the
chemical type of pain.
Prostaglandins and
substance P enhance the
sensitivity of pain endings
but do not directly excite
them.
Hyperalgesia:
The skin, joints, or muscles that have already been
damaged are unusually sensitive. A light touch to a
damaged area may elicit excruciating pain;
Primary hyperalgesia occurs within the area of
damaged tissue;
Secondary hyperalgesia occurs within the tissues
surrounding a damaged area.
2. Localization of Pain
•Superficial Somatic Pain arises from skin areas
•Deep Somatic Pain arises from muscle, joints,
tendons & fascia
•Visceral Pain arises from receptors in visceral organs
–localized damage (cutting) intestines causes no pain
–diffuse visceral stimulation can be severe
•distension of a bile duct from a gallstone
•distension of the ureter from a kidney stone
3. Fast and Slow Pain
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Most pain sensation is a combination of the two
types of message.
– If you prick your finger you first feel a sharp pain
which is conducted by the A fibres,
– and this is followed by a dull pain conveyed along C
fibres.
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Fast pain (acute)
– occurs rapidly after stimuli (.1 second)
– sharp pain like needle puncture or cut
– not felt in deeper tissues
– larger A nerve fibers
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Slow pain (chronic)
– begins more slowly & increases in intensity
– in both superficial and deeper tissues
– smaller C nerve fibers
spinothalamic
pathway
to reticular
formation
Aδ nerve
C nerve
nociceptor
nociceptor
Impulses transmitted to spinal cord by
– Myelinated Aδ nerves: fast pain (80 m/s)
– Unmyelinated C nerves: slow pain (0.4 m/s)
somatosensory
cortex
thalamus
spinothalamic
pathway
reticular
formation
Impulses ascend to somatosensory cortex via:
– Spinothalamic pathway (fast pain)
– Reticular formation (slow pain)
4. Visceral pain
Notable features of visceral pain:
Often accompanied by strong autonomic and/or
somatic reflexes
Poorly localized;
may be “referred”
Mostly caused by distension of hollow organs or
ischemia (localized mechanical trauma may be
painless)
Afferent innervation of the viscera.
Often anatomical separation nociceptive innervation (in
sympathetic nerves) from non-nociceptive
(predominantly in vagus).
Many visceral afferents are specialized nociceptors, as
in other tissues small (Ad and C) fibers involved.
Large numbers of silent/sleeping nociceptors, awakened
by inflammation.
Nociceptor sensitization well developed in all visceral
nociceptors.
Referred pain
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Pain originating from
organs perceived as
coming from skin
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Site of pain may be
distant from organ
Convergence theory:
This type of referred pain occurs
because both visceral and
somatic afferents often converge
on the same interneurons in the
pain pathways.
Referred pain
Excitation of the somatic
afferent fibers is the more usual
source of afferent discharge,
so we “refer” the location of
visceral receptor activation to
the somatic source even though
in the case of visceral pain.
The perception is incorrect.
The convergence of
nociceptor input from the
viscera and the skin.
5. “Pain Gate” Theory
Melzack & Wall (1965)
A gate, where pain impulses can be “gated”
The synaptic junctions between the peripheral nociceptor
fiber and the dorsal horn cells in the spinal cord are the
sites of considerable plasticity.
A “gate” can stop pain signals arriving at the spinal cord
from being passed to the brain
– Reduced pain sensation
– Natural pain relief (analgesia)
descending nerve
fibers from brain
pain pathways
axons from touch
receptors
axons from nociceptors
“THE PAIN GATE”
opioid-releasing
interneuron
How does “pain gate” work?
The gate = spinal cord interneurons that
release opioids.
The gate can be activated by:
– Simultaneous activity in other sensory (touch)
neurons
– Descending nerve fibers from brain
Applications of pain gate
Stimulation of touch fibres for pain relief:
– TENS (transcutaneous electrical nerve stimulation)
– Acupuncture
– Massage
Release of natural opioids
– Hypnosis
– Natural childbirth techniques
6. Pain Relief
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Aspirin and ibuprofen block formation of
prostaglandins that stimulate nociceptors
 Novocain blocks conduction of nerve
impulses along pain fibers
 Morphine lessen the perception of pain in
the brain.