Neurophysiology Series

SENSORY FUNCTION
OF THE NERVOUS SYSTEM
www.physiology.sdu.edu.cn

By Sawiji Amani
Mobile phone: 081 328 028333
E-mail: sawijiamani@gmail.com

Basic Sciences Department

Muhammadiyah Gombong University
Central Java Indonesia
 I Sensory pathways
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,
A
temperature)

B: Pacinian corpuscle (pressure)

B C C: Meissners corpuscle (touch)

D: Muscle spindle (stretch)

D
Sensory receptors
Ruffini's endings respond to tension and stretch in the skin
 Sensory receptors

Sensory receptors: organs which detect

sensory stimuli .

Sensory stimuli: sensation modality (touch,

sound, light, pain, cold, and warmth..etc)
 Sensory receptors
Mechanoreceptors: detect mechanical compression or
stretching of tissues
Thermoreceptors: detect changes in temperature
Nociceptors (pain receptors): detect tissue damage
( physical or chemical damage)
Chemoreceptors: detect taste in the mouth, smell in the nose,
oxygen level ..etc.
Electromagnetic receptors (photoreceptor): detect
light on the retina
 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

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 Pain, temperature,
some touch
Spinal cord
Spinothalamic damage
Left
spinothalamic pathway spinal cord injury

Loss of sense of:

Touch
Pain
Warmth/cold
in right leg
 2.2 Dorsal column pathway

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
Medial
Dorsal column
lemniscus Large sensory nerves:
Touch, vibration, two-point
Spinal cord
discrimination, proprioception
 Left
dorsal column spinal cord injury

Dorsal pathway

column
damage

Loss of sense of:

touch
proprioception
vibration
in left leg
 Dorsal column damage

Sensory ataxia

Patientstaggers; cannot
perceive position or
movement of legs

Visual clues help movement

 Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing,
and Allied Health, Seventh Edition. 2003 by Saunders, an imprint
of Elsevier, Inc. All rights reserved.

ataxia[ah-takse-ah]failure of muscular
coordination; irregularity of muscular
action. adj., adj atactic, ataxic.
sensoryataxia: ataxia due to loss of
proprioception (joint position sense),
resulting in poorly judged movements and
becoming aggravated when the eyes are
closed.
 Central
Pathways
Sensory pathways cross the bodys midline (Silverthorn: 2007)
 3.3 Spinocerebellar pathway
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
Cerebellar ataxia : ataxia due to disease of
the cerebellum.
Clumsy movements
Incoordination of the limbs (intention
tremor)
Wide-based, reeling gait (ataxia)
Alcoholic intoxication produces similar
effects!
 4. Somatosensorycortex
Located in the postcentral gyrus of the
human cerebral cortex.
LobusParietalis:Fungsi&AsosiasiSomatosensoris
Gyrus postsentral : kortekssomatosensoriprimer
Sentuhan/raba lembut, tekanan, nyeri & suhu, sensasi umum di kepala
Sensory homunculus (representasi disproporsional)
1) Eachsideof Spatial orientation of signals.
thecortex
receives
sensory
information
exclusively
fromthe
oppositesideof
thebody
(theexception:
thesameside
oftheface).
2)Thelips,face Spatial orientation of signals.
andthumbare
representedby
largeareasinthe
somaticcortex,
whereasthetrunk
andlowerpartof
thebody,relatively
smallarea.

3)Theheadinthemostlateralportion,andthe
lowerbodyispresentedmedially
Sensory homunculus (representasi disproporsional)
Sensory homunculus (representasi disproporsional)
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?
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
1. Nociceptors

free nerve endings in

skin respond to
noxious stimuli
 Nociceptors
Nociceptorsare 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,andproteolytic
enzymescanexcitethe
chemicaltypeofpain.
Prostaglandinsand
substancePenhancethe
sensitivityofpainendings
butdonotdirectlyexcite
them.
 Hyperalgesia:
Theskin,joints,ormusclesthathavealreadybeen
damagedareunusuallysensitive.Alighttouchtoa
damagedareamayelicitexcruciatingpain;

Primary hyperalgesiaoccurswithintheareaof
damagedtissue;
Secondary hyperalgesiaoccurswithinthetissues
surroundingadamagedarea.
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

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.
 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
 spinothalamic
pathway

to reticular
formation

A nerve C nerve

nociceptor
nociceptor

Impulses transmitted to spinal cord by

Myelinated A nerves: fast pain (80 m/s)
Unmyelinated C nerves: slow pain (0.4 m/s)
 somato-
sensory
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 referred pain
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
Pain originating from
organs perceived as
coming from skin

Site of pain may be

distant from organ
Convergence theory:

Thistypeofreferredpainoccurs
Referred pain
becausebothvisceraland
somaticafferentsoftenconverge
onthesameinterneuronsinthe
painpathways.

Excitationofthesomatic
afferentfibersisthemoreusual
sourceofafferentdischarge,

sowereferthelocationof
visceralreceptoractivationto
thesomaticsourceeventhough
The convergence of
inthecaseofvisceralpain.
nociceptor input from the
viscera and the skin.
Theperceptionisincorrect.
 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

axons from touch

receptors
pain pathways
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
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.
 Phantom Limb Sensation
(Tortora & Derrickson, 2006:552)

Patients who have had a limb amputated

may still experience sensations such as
itching, pressure, tingling, or pain as if the
limb were still there.
This phenomenon is called PhantomLimb
Sensation.
Why so?
 Some Explanations
(Tortora & Derrickson, 2006:552)

1. The cerebral cortex interprets impulses arising in

the proximal portions of sensory neurons that
previously carried impulses from the limb as
coming from the nonexistent (phantom) limb.
2. The brain itself contains networks of neurons
that generate sensations of body awareness.
3. Neurons in the brain that previously received
sensory impulses from the missing limb are still
active, giving rise to false sensory perceptions.
 (Tortora & Derrickson, 2006:552)

Phantom limb can be very distressing to an

amputee.
Many report that the pain is severe or
extremely intense, and that it often does not
respond to traditional pain medication therapy.
In such cases, alternative treatments may
include electrical nerve stimulation,
acupuncture, and biofeedback.
 Analgesia: Relief from Pain
(Tortora & Derrickson, 2006:553)

Pain sensations sometimes occur out of proportion

to minor damage, persist chronically due to an
injury, or even appear for no obvious reason.
In such cases, analgesia (an- = without; -algesia =
pain) or pain relief is needed.
Analgesic drugs such as aspirin and ibuprofen (for
example, Advil or Motrin) block formation of
prostaglandins, which stimulate nociceptors.
 (Tortora & Derrickson, 2006:553)

Local anesthetics, such as Novocaine, provide

short-term pain relief by blocking conduction of
nerve impulses along the axons of first-order pain
neurons.
Morphine and other opiate drugs alter the quality of
pain perception in the brain; pain is still sensed, but
it is no longer perceived as being so noxious.
Many pain clinics use anticonvulsant and anti
depressant medications to treat those suffering from
chronic pain.