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8/4/2019 Nervous System Part Three Sensory Function
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Part 3
Sensory Function of the Nervous
System
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I Sensory pathways
Sensory systems allow us to detect, analyze andrespond 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
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1. Sensory receptors
A: Free nerve endings (pain, temperature)
B: Pacinian corpuscle (pressure)
C: Meissners corpuscle (touch)
D: Muscle spindle (stretch)
A
B C
D
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Ruffini's endings respond to tension and stretch in the skin
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2. Sensory pathways: 3neurons
1st: enters spinal cord from periphery
2nd: crosses over (decussates), ascends
in spinal cord to thalamus
3rd
: projects to somatosensory cortex
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2.1 Spinothalamic pathway
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
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spinothalamicpathway
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Spinothalamic Pathway
Small sensory fibres:
Pain, temperature,
some touch
Primary somatosensorycortex (S1)
Thalamus
Medulla
Spinal cord
Spinothalamictract
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Spinothalamic damage
spinothalamic pathway
Leftspinal cord injury
Loss of sense of:TouchPainWarmth/coldin right leg
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2.2 Dorsal column pathway
Carries fine touch, vibrationand conscious proprioceptionsignals
1st neuron enters spinal cord
through dorsal root; ascendsto medulla (brain stem)
2nd neuron crosses over inmedulla; ascends to thalamus
3rd neuron projects tosomatosensory cortex
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Two-Point Discrimination
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dorsalcloumn
pathway
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Dorsal column pathway
Large sensory nerves:
Touch, vibration, two-point
discrimination, proprioception
Primary somatosensorycortex (S1) in parietal
lobe
Thalamus
MedullaMediallemniscus
Spinal cord
Dorsal column
Dorsal columnnuclei
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Dorsal
columndamage
dorsal columnpathway
Leftspinal cord injury
Loss of sense of:touchproprioceptionvibrationin left leg
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Dorsal column damage
Sensory ataxia
Patient staggers; cannotperceive position or
movement of legs
Visual clues help movement
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Central
Pathways
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3.3 Spinocerebellar pathway
Carries unconsciousproprioception 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
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Spinocerebellar tract damage
Cerebellar ataxia
Clumsy movements
Incoordination of the limbs (intentiontremor)
Wide-based, reeling gait (ataxia)
Alcoholic intoxication produces similareffects!
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4. Somatosensory cortex
Located in the postcentral gyrus of thehuman cerebral cortex.
S i l i i f i l
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Spatial orientation of signals.1) Each side of
the cortex
receivessensory
information
exclusivelyfrom the
opposite side of
the body
(the exception:
the same side
of the face).
S ti l i t ti f i l
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Spatial orientation of signals.2)The lips, face
and thumb are
represented by
large areas in the
somatic cortex,
whereas the trunkand lower part of
the body, relatively
small area.
3)The head in the most lateral portion, and the
lower body is presented medially
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II . Pain
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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
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Why feel pain?
Gives conscious awareness of tissue
damage
Protection:
Remove body from danger
Promote healing by preventing further damage
Avoid noxious stimuli
Elicits behavioural and emotional responses
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free nerve endings in
skin respond to
noxious stimuli
1. Nociceptors
N i
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Nociceptors Nociceptors are special receptors that respond only
to noxious stimuli and generate nerve impulseswhich the brain interprets as "pain".
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Adequate Stimulation
Temperature
Mechanical damage
Chemicals (released fromdamaged tissue)
Bradykinin, serotonin,histamine, K+, acids,acetylcholine, and proteolyticenzymes can excite the
chemical type of pain.
Prostaglandins andsubstance P enhance thesensitivity of pain endings
but do not directly excitethem.
Nociopectors
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Hyperalgesia:
The skin, joints, or muscles that have already beendamaged are unusually sensitive. A light touch to a
damaged area may elicit excruciating pain;
Primary hyperalgesia occurs within the area ofdamaged tissue;
Secondary hyperalgesia occurs within the tissuessurrounding a damaged area.
2 L li i f P i
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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 organslocalized 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
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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 painwhich is conducted by the A fibres,
and this is followed by a dull pain conveyed along C
fibres.
3. Fast and Slow Pain
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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 Slow pain (chronic)
begins more slowly & increases in intensity
in both superficial and deeper tissues smaller C nerve fibers
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Impulses transmitted to spinal cord by
Myelinated A nerves: fast pain (80 m/s)
Unmyelinated C nerves: slow pain (0.4 m/s)
nociceptor
nociceptor
A nerve C nerve
spinothalamicpathway
to reticularformation
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Impulses ascend to somatosensory cortex via:
Spinothalamic pathway (fast pain)
Reticular formation (slow pain)
reticularformation
spinothalamicpathway
thalamus
somato-sensory
cortex
4 Vi l i
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4. Visceral pain
Notable features of visceral pain:Often accompanied by strong autonomic and/orsomatic reflexes
Poorly localized;
may be referred
Mostly caused by distension of hollow organs orischemia (localized mechanical trauma may bepainless)
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Afferent innervation of the viscera.
Often anatomical separation nociceptive innervation (insympathetic nerves) from non-nociceptive(predominantly in vagus).
Many visceral afferents are specialized nociceptors, asin other tissues small (Ad and C) fibers involved.
Large numbers of silent/sleeping nociceptors, awakened
by inflammation.Nociceptor sensitization well developed in all visceralnociceptors.
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Convergence theory:
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Convergence theory:
This type of referred pain occurs
because both visceral and
somatic afferents often convergeon the same interneurons in the
pain pathways.
Excitation of the somaticafferent 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 ofnociceptor input from theviscera and the skin.
Referred pain
5 P i G t Th
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5. Pain Gate TheoryMelzack & 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 thesites 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)
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descending nervefibers from brain
axons from touchreceptors
axons from nociceptors
THE PAIN GATEopioid-releasinginterneuron
pain pathways
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How does pain gate work?
The gate = spinal cord interneurons thatrelease opioids.
The gate can be activated by:
Simultaneous activity in other sensory (touch)neurons
Descending nerve fibers from brain
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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
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