SUBJECT: PHYSIOLOGY
TOPIC: Neurophysiology of Somatic Sensations
LECTURER: DR. SIMBULAN
DATE: FEBRUARY 2011
Discussion Outline:
i. Overview of somatic sensations
ii. Cutaneous Sensory Physiology
a. Skin Mechanoreceptors
b. Thermoreceptors
iii. Proprioceptors –also are somatosensory
(will be discussed during the Reflex Lecture)
a. Muscle spindle
b. Golgi tendon organs
*these two are the most studied
proprioceptors, though they are also
somatosensory receptors
*There are also other proprioceptors in skin
and joint/muscle, but we will not be dealing
with them much anymore
iv. Cutaneous & Visceral Pain Receptors
(Nociceptors & Intro to Pain Physiology) -
Pain receptors and various ascending fibers
which may take the fast pain / slow pain,
and recent advances in introductory pain
physiology
Two Well Studied Endogenous Pain Control Systems:
1. Gate control system
 by Dr. Walden Melzack
 discovered in 1960’s
- know the lateral inhibition mechanism behind
this GCC/spinal gating
- you may read more about this in your book
2. Descending pain inhibition system (late 1970-
1980’s)
**these two are briefly described in handout diagram
Objectives:
 Know the features & functions of receptors
 Know how adequate stimuli is converted to changes
membrane conductance (receptor potential)
 Know the size of receptive field (small/large;
contribution in characterizing sensory stimuli
 Know how increasing stimulus intensity is expressed
in terms of increasing spike discharges
 Know the Central & Peripheral Mechanisms of pain
and analgesia
 distinguish fast pain, slow pain, referred pain,
projected pain
 gating theory, opiod and non-opiod mechanism of
endogenous pain control
 short definitions: hyperalgesia, allodynia, muscle
radiating spasm, congenital insensitivity to pain,
PHYSIOLOGY: Neurophysiology of Somatic Sensations
phantom limb/phantom pain and peripheral and
central mechanisms theories to explain this
phenomenon
 itch vs. tickle vs. pain
Review:
Dorsal Root Ganglion (DRG)
 1st order neuron of the somatosensory system,
whether it is for crude touch, pressure, pain,
temperature, proprioception, fine touch, 2 point
determination)
 If from face region, what is the 1st order sensory
neuron?
2 general classes of DRG neurons
(innervate various somatosensory receptors):
1. Large DRG neurons
 Large soma, large axon (from single
branching from soma, divides into 2
processes)
o Peripheral – innervates the
sensory receptors
o Central – enter the dorsal horn
(posterior gray horn) of spinal
cord
 they are myelinated (not all myelinated
are large, refer to Type A delta fibers
described below)
 Ex. Neurons that give rise to Type A beta,
Type A delta, and Type A gamma fibers
 Sensory modalities involved:
Proprioception, Fine Touch, Pacinian
Corpuscles, etc.
2. Small DRG Neurons
 Neurons that give rise to:
o C Fibers
o Type A delta fibers (myelinated)
= if compared with other Type A
afferent fibers, A delta are
smaller
 Sensory Modalities involved: Most from
Anterolateral system (but not all, only
majority) – some experimental literatures
state that fine touch afferents send
‘some’ collateral to ALS; also, pain too
sends ‘some’ collaterals to the medial
lemniscal pathway.
* keyword: “some”
Page 1
Fast Pain = generally part of small DRG, with Type A Lecture Proper:
delta fibers, myelinated but smaller in diameter (smaller,
I. Overview
as compared with large DRG axons)
Ascending Tracts
Slow pain = C fibers innervated
 Anterolateral System, composed of :
Crude Touch = difficulty to localize; innervated by C
fibers 1. Lateral Spinothalamic Tract – pain and
temperature
Fine Touch = uses vibratory sensors, those specialized 2. Anterior (Ventral) Spinothalamic Tract –
for precise stimulus localization such as Merkel’s disks, touch and pressure
Meissners, Ruffini’s, Pacinian, Hair Cells
*recall their sites of decussation, thalamic nuclei
*however based on actual experimental observation (ex: destination, cerebral cortex destination, also, look
histological), fine touch modalities are discovered to at images of the sensory homunculus
have ‘some’ Type A delta fibers (but still, mostly have
Sensory Homunculus – regional specification can
larger diameters)
change (amputees developing the remaining limb’s
*thermal receptors = predominantly a delta and c fibers capabilities); Size of cortical receptive fields =
proportional to the density of receptors in the
Dr. Simbulan: this can be confusing in terms of representative region. (Fingers: have high density of ss
innervation. Generally, small myelinated and receptors)
unmyelinated C fibers predominate nociceptors;
proprioception generally A beta and A alpha Guyton further divided the spinothalamic tract into:
a. Paleospinothalamic – connecting mostly to
Still Confused? Just remember this: brainstem, then to intralaminar thalamic nuclei
 Proprioceptors: before going to Cerebral Cortex; generally
o large diameter, myelinated related to affective/emotional aspects of pain
o Aβ, Aα b. Neospinothalamic – associated to fast pain
 Crude touch, pain, temperature:
o small, unmyelinated  Dorsal Column / Medial Lemniscal System
o Group 4 or Type C fibers –fine touch, proprioception
 Fine touch, vibration, pressure:
o large, myelinated
Effects of Damage to Somatosensory cortex
o Group 2, or the rest of Type A
 A few Thermoreceptors: > Severely damaged Area 312 = contralateral loss of
o Aδ, C sensation; however, based on experiments, actually:
 *somatic motor neurons (ventral horn):
o Aα  tactile sensations – all fine tactile is generally
abolished (esp. at contralateral side); crude
Diameter Type Modality
touch is recovered after a period of time
(μm)  Pain, temperature – left generally intact
12-20 Aα Proprioception
Hence, we can conclude that:
5-12 Aβ Fine touch, Pressure • in fine touch: cortex is very important
• in pain, temp: awareness center is below
3-6 Aγ Muscle Spindles cortex (can even be at thalamus), though there
are no definite studies as to where it is exactly.
2-5 Aδ Pain, Cold, crude touch
It is just somewhere below the cortex. The role
<3 B Preganglionic Autonomic of cortex perhaps is mainly on the localization
of the pain or temperature stimulus.
0.4-1.2 C Pain, Temperature, etc.
> Lesions to Area 5 AND 7
= Sensory Association Cortex Lesion)
= astereognosis; inability to identify an object if
touched when blindfolded

PHYSIOLOGY: Neurophysiology of Somatic Sensations Page 2

 Somatic Senses Pathways Scientists were also able to identify via
(ALS or Medial Lemniscus) microneurography whether the receptors have small or
large receptive fields.

Ventrobasal Nuclei Which size of receptive field gives more exact

(VPM – if from head, neck) information about the location of the stimulus? Small!
(VPL – if from rest of the body)
Naming Convention for Mechanoreceptors

Tactile Receptor Adaptation Receptive Field Code

Area 312
(Anterior Parietal Cortex) 1. Pacinian Corpuscle Fast large FA-II

2. Meissner’s Corpuscle Fast small FA-I

Sensory Association Cortex
3. Merkel’s Disk Slow small SA-I
(Posterior Parietal Cortex)
- helps identify objects only by touching via higher 4. Hair Follicle Endings Fast small FA-I
order processing (stereognosis)
5. Ruffini’s Endings Slow large SA-II
- makes holistic image of the object
FA = Fast Adapting
II. Sensory Receptors of Skin SA = Slowly Adapting
I = small receptive field
Cutaneous Receptors
II = large receptive field
– can be found in both hairy/hairless skin
>>>>>Slowly vs. Fast Adapting Receptors
– studied via microneurography (thus, it was - see last page
studied in isolated nerves from animals/humans,
without actually exposing the nerves. They just
stimulate nerve ending above skin with some pressure (want tabular form? See final page)
stimuli (or other stimuli). Microelectrodes are inserted 1. Pacinian Corpuscle (FA-II)
to actually impinge on the isolated nerve itself. Action  Rapidly adapting
potentialns are recorded. It is with this technique that  Studied well via microneurographic
we were able to identify the thresholds for various techniques
 Onion-like lamellar capsule (about 1mm in
mechanoreceptors, as well as their receptive fields, and
diameter)
whether the receptors are slowly or rapidly adapting.
✪ Speed of Adaptation: very rapid
Receptor potentials as stimulus intensity is increased
(ex: from 0.1 to 0.6 Newton) = increasing amplitude. ✪ Receptive Field: Large (hence, not accurate in
localizing stimulus source)
When the action potentials were recorded from the
axon itself where checked, they have increasing ✪ Encoded Sensation: touch, vibration
(acceleration detector)
discharge frequency
✪ Afferents, location: generally Aβ (some Aα); skin
 Aβ = large, myelinated, group 2
In short:
Increase in stimulus intensity (skin
“Increase stimulus intensity, increase amplitude of deformation is the stimulus)
receptor potential, increase discharge frequency of
sensory nerve.”
Stimulus intensity
maintained constant.

There is only discharge only

when there is increase in
intensity. After that, there
Discharge is no more response

PHYSIOLOGY: Neurophysiology of Somatic Sensations Page 3

Pacinian Corpuscles only become really active (with
higher discharge frequency) when stimulus frequency is
increased within this frequency range: 200-300 Hz.
(Create stimulus within this range, and this is the only
time the sensory nerve will have higher discharge
frequency)
2. Meissner’s Corpuscle (FA-I)
 Rapidly adapting
 Studied well via microneurographic
techniques
✪ Speed of Adaptation: very rapid
✪ Receptive Field: small (hence, accurate in
localizing stimulus source)
✪ Encoded Sensation: speed of stimulus
application, low freq vibration sensors (like
pacinian, though meissner’s have lower
sensibility: 30-40Hz)
✪ Afferents, location: Aβ (group2); fingertips, lips,
skin, even at sexual erectile tissues, glans penis,
etc.
3. Ruffini Endings (SA-II)
 Slowly adapting
 Studied well via microneurographic
techniques
✪ Speed of Adaptation: slow
✪ Receptive Field: large (hence, not accurate in
localizing stimulus source)
✪ Encoded Sensation: magnitude and duration of
stimulus (touch pressure); because it is slowly
adapting, it can give accurate description
magnitude and duration… unlike those that
are rapidly adapting
✪ Afferents, location: Aβ (group2), with some Aα
according to some literature ; covered by
liquid filled collagen
4. Merkel’s Disk (SA-I)
 Slowly adapting
 Studied well via microneurographic
techniques
 An independent cell; a specialized epithelial
cell that releases a chemical messenger
(which acts like a neurotransmitter),
activating sensory nerve endings that
synapse with them.
PHYSIOLOGY: Neurophysiology of Somatic Sensations
✪ Speed of Adaptation: slow
✪ Receptive Field: small (hence, accurate in
localizing stimulus source)
✪ Encoded Sensation: localization of stimulus
(touch pressure)
✪ Afferents, location: Aβ (group2); high density
in fingertips, lips, many skin areas
5. Hair Follicle Endings
 Rapidly adapting
 Studied well via microneurographic
techniques
 Practical example: when you wear your
clothes, at first you feel them on you, but
as time passes, you won’t even feel them
(you won’t be constantly conscious of it)
Of course, when you move, you stimulate
these hair endings a bit to produce some
spike discharges so you can feel it as you
move
✪ Speed of Adaptation: rapid
✪ Receptive Field: small (hence, accurate in
localizing stimulus source)
✪ Encoded Sensation: light touch flutter; low
vibration sensors (30-40 Hz, like Meissner’s)
✪ Afferents, location: Aβ (group2)
6. Tactile Discs
7. Other Cutaneous Receptors
Two point threshold
 Two point
discrimination
threshold
 Using a compass,
or any tool with 2
points
 Smallest tip separation for which the subject
can tell that there are two stimulus source
points without looking at them
>> High two point threshold = low sensitivity
(ex: scapular region, back of neck)
>> Low two point threshold = high sensitivity
(ex: fingertips)
Page 4
Spatial resolution
 Can be extracted using the values of the two
point threshold
 the inverse/reciprocal of the two point
threshold
 if two point threshold is 70; spatial threshold is
1/70
 the higher the two point threshold; the lower
the spatial resolution
 more sensitive areas will have higher spatial
resolution
I cannot find the image that Dr.
Simbulan flashed during his
lecture. Sorry
*The ones with highest spatial resolution (low 2 pt
threshold) = fingertip; also has high density of
mechanoreceptors with small receptive field and low
density of mechanoreceptors with large receptive field.
Transduction Mechanism of Mechanoreceptors
Simply stretching the extracellular matrix of the skin
would stretch the cytoskeletal structures which open up
the mechanically gated ion channels allowing cation
influx, causing initial depolarization (receptor potentials
form)
Temperature = generally group a delta and c fibers;
Thermal Spots
Hairy skin has larger thermal spots than hairless skin
PHYSIOLOGY: Neurophysiology of Somatic Sensations
A Monkey Experiment using Braille (to evaluate
various mechanoreceptors)
 Pattern recorded closely resembles Braille: SA-
I (Merkel’s disc)
 More or less resembles the Braille: FA-I
(Meissner’s Corpuscle)
 The CNS cannot describe it, no idea at all: SA-II
(Ruffini’s Endings), FA-II (Pacinian Corpuscles)
*the characteristic common with Merkel’s and
Meissner’s = both have small receptive field, that’s why
they are good in localizing stimulus (hence, creating a
closer image of it)
**You may try to look for the image related to the
monkey-braille experiment, if you are having a hard
time visualizing it.
Recent findings on temperature sensation
transduction mechanisms
 There are receptors for ATP (ATP is released
by surrounding tissues, exciting the free nerve
endings that are sensitive to warm stimulus)
o P2X receptors = purinergic receptors
which are activated ATP released from
surrounding tisssues; mediate
moderate heat sensations
 There are also receptors found in cold
receptor free nerve endings
o CMR (cold and methol sensitive
receptor)
‘
Page 5

*if you go higher (temp), the activity of the cold
receptors will dive down (same happens for warm
receptors)
*If temperature is increased beyond 45 degrees, before
sensory nerves become denatured, there will be an
increase in discharge frequency… results to paradoxical
cold sensation. (Principle: cold receptors are briefly
active before they are inactivated; the pain sensation is
from the pain receptors) Prolong the exposure to high
temperature, and the cold receptors will be destroyed.
Pain receptors will be activated (slow pain if there will
be swelling and blisters forming)
*example: accidentally touching a hot iron, you will feel
brief coldness, then pain (try it!)
>>Thermal Stimulus (34 degrees30 degrees34
degrees)
>>Cold Fiber = Cold sensitive free nerve endings
>>Warm Fiber = Heat sensitive free nerve endings
*However, these two cannot give any responses to
absolute temperature, only to transient changes in
temperature
PHYSIOLOGY: Neurophysiology of Somatic Sensations
There are specific types of nociceptors for every
damaging stimulus:
 Cold nociceptors
 Hot nociceptors
 Mechanonociceptors
 Chemonociceptors
Are “receptors” used in different ways? Cold receptor? Pain Receptor?
The word “Receptor” can describe:
1. a part of a sensory nerve ending, or specialized
epithelial cell that causes changes to
membrane conductance in response to an
adequate stimulus
2. a transmembrane protein in the cell
membrane that may have different function
(can be an enzyme, an ion channel, binds to
chemical messenger)
*don’t be confused when the word “receptor” is used in
a statement to describe different things
The opposite occurs when the
temperature is increased
* Hence, the CNS uses both warm and cold fibers to
respond to cold or warm stimulus (if stimulus is cold,
heat sensitive free nerve endings also acts, v/v.)
Trivia:
According to new version of Ganong: ipsilateral insular
cortex is a possible new sensory cortex for thermal
sensation
Page 6
Questions:
1. Difference of pain receptors from others:
signals potential threat/damage
2. The importance of pain receptors? They lead to
the eventual removal of damaging stimuli
3. When is pain harmful? If it is chronic in nature
that it already disturbs personal and social life,
or even causes loss of sensation leading to self
mutilation
Chronic Pain related to illnesses
 Diabetes = leads to peripheral neuropathies;
leads to hyperactivity and degeneration of
sensory nerves, causing chronic pain
 Whiplash syndrome = from injury arising from
neck, complains for a long period of time
 Spinal Nerve Problems = if vertebrae is
degenerating; may cause chronic pain
 Chronic Headache experiences = like migraine
 Onset of changes of physiologic states =
dysmenorrhea (possibly with headache)
III. Cutaneous and Visceral Nociceptors
 Cutaneous Nociceptors (Skin receptors)
o A delta (fast pain) group III
o C fibers (slow pain) group IV
*Specific for damaging mechanical,
chemical, or thermal stimuli
Question: If you are to isolate touch receptors: merkel’s,
meissner’s, ruffini’s, pacinian (assuming you can isolate
them) –then increase stimulation intensity. What will
be the sensation felt (touch only, or both touch and
pain)?
Answer: Only touch sensation will be generated; no
pain sensation will be felt. (See Mullerian Doctrine of
Specific Nerve Energies). Overstimulation will only lead
to pain if the touch receptors are not isolated and are
adjacent to pain receptors. Thus, the overstimulation
hypothesis is countered.
Mullerian Doctrine of Specific nerve energies.
- The sensation which is generated by
stimulating a sensory pathway or receptor is due to the
fact that there is a specialized receptor for that
particular sensation. And of course, the sensation
generated is basically due to the central connections of
this sensory pathway
- for one specific type of sensation there is one
type of sensory receptor with its own sensory ascending
pathway to a part of the brain
PHYSIOLOGY: Neurophysiology of Somatic Sensations
Overstimulation hypothesis
- when you stimulate a receptor lightly, you
only cause touch and when you stimulate it at higher
intensity, temperature at higher still, possibly tickle and
more, pain.
Labeled Line Mechanism
- No matter how specialized sensory receptor is,
if there are no central connections no sensory
experience. That kind of central connection component
is called labeled line mechanism—it is a little bit of an
extension of this older doctrine.
 Visceral Nociceptors
o Primarily innervated by C fibers (slow)
o Periosteum, joint Surfaces, dura mater,
tentorium, cranial vault
o Most are associated with Referred pain
Referred Pain
- there are corresponding surfaces of the
body wherein pain is referred to by various injuries or
some inflammatory conditions of internal organs.
 Muscle nociceptors
o Primarily A delta (III) and C type (IV)
o Ischemic pain (blood unable to cope with
contraction
o Basically, much of these receptors are
activated as a result of occlusion of blood
supply in the muscle tissue contributing to
relief of other sensitizing chemicals like
potassium in a so-called Louis factor so
this can either be experienced in skeletal
or cardiac muscles which can activate
these muscle pain receptors.
o the adequate stimuli in transduction
mechanisms involved for pain pathways,
generally speaking, damaged cells can
induce the release of various
neurochemicals or other tissue chemicals
of non-neural nature which would
sensitize or activate numerous nerve
endings. So in addition to histamine, you
have potassium, and hydrogen ions.
Activators (Tissue Chemicals) that activate nociceptors
o In addition to histamine or bradykinin,
which are released from damaged tissues
and can activate these damaged
nociceptors, there are other tissue
chemicals of both neural and nonneural
nature which can activate various pain
nerve ending.
o Synthesized by polypeptides
 Cholecystokinin
 Opiods
 Neurokinin
Page 7
 o Non neural
 Histamine
 Bradykinin
 Acetylcholine
 ATP
 Etc.
o Neural
 What are they?
= And they bind to their corresponding receptors on
pain nerve endings so it seems the pain system is really
a primitive system which can respond to various
chemicals. So even if you fail to synthesize one kind of
chemical due to gene mutation, still, there are other
chemicals released from damaged tissue which can
activate the pain system. So they are not as highly
specialized as the other pain systems.
Other neurobiological findings will be specialized
receptors which can activate some endings. For
example, the sili.
 The component of some chili sauce is a
capsaicin, a molecule which activates your
vanilloid, your vr1 receptor. The receptor itself
is activated by temperature beyond 43
degrees centigrade. Probably some kind of hot
nociceptors.
 In addition, there are also other kinds of
membrane receptors called vrl1 receptor
which is non-capsaicin sensitive and is also
activated by changes of thermal stimulus
beyond 50 degrees centigrade.
 So these vrl1 is supposed to be found in c
fibers. However, data does not actually discuss
whether they come from a delta or c fibers.
Remember:
o VR1 = capsaicin sensitive
o VRL1 = non capsaicin sensitive
Activation of Pain System
- as long as there is damage to the tissue
- a nerve ending can stimulate itself
(autostimulation of pain)by releasing chemicals such as
substance P.
Interaction of Bradykinin with other neurochemicals
and tissue chemicals in sensitizing joint tissue during
inflammation (such as arthritis)
1. Damaged tissue releases bradykinin.
2. Bradykinin will stimulate a corresponding receptor
(like B2, a metabotropic receptor)
3. Other sensitizing chemicals will be released
4. How bradykinin interacts with them determines the
excitation of the sensory endings (complex cocktail
of chemicals + prostaglandins)
PHYSIOLOGY: Neurophysiology of Somatic Sensations
Question: if prostaglandins are the predominant
chemicals, what kind of analgesics would be most
effective?
Answer: Your aspirin-like drugs. They are prostaglandin
synthesis inhibitors. They actually inhibit the synthesis
of prostaglandin.
5. histamine is released from mast cells, activating
histamine receptors
6. Serotonin is also released. It is a known active
ingredient in inflammatory tissues, in inflamed
joints.
7. The role of sympathetic system in pain, especially if
there’s nerve injury, is induced.
Uninjured Nerve
What is known is that many pain nerves as well as
ordinary somatosensory pain nerves are not highly
excitable at the basal state, if they are not injured.
Injured Nerve
But when they are injured, what has been found out is
that many of these pain nerves as well as ordinary pain
nerve endings upregulated their membrane molecular
receptors for norepinephrine (either in the soma or in
the peripheral nerve endings).
The alpha adrenoreceptor is a receptor subtype
for norepinephrine. When they upregulate this receptor,
they become sensitive to circulating or basal
concentrations of norepinephrine in the blood, in the
plasma. And then they would possibly reach these free
nerve endings. So upregulation of these norepinephrine
receptors can make them excitable and that is why
many of these nerve injuries are very difficult to
suppress the pain so what some pain doctors would do
is to use blocking agents for some alpha norepinephrine
receptor.
Role of norepinephrine receptors in nerve endings of
pain system
Again, another important polypeptide is substance P
which is not only released in the soma of dorsal horn,
but they’ve been found to be released in free nerve
endings in inflamed tissue and they can also cause
sensitization of pain afferents. Then hydrogen ions
when the tissues become more acidic as a result of
damaged tissue so there are protons here and then of
course the release of free radicals like H2O2 from
damaged tissue can also cause activation of nerve
endings.
H2O2 – increases pain sensitivity
H+ – acidity also increases pain sensitivity
Bradykinin cascade – metabotropic; uses G protein and
Phospholipase C
Page 8
Fast Pain vs. Slow Pain
FAST (First) PAIN SLOW (Second) PAIN
“initial” “delayed”
Aδ fibers C fibers
Discrete Burning sensation
Sharp dull
Well localized Poorly localized
Neospinothalamic = associated with fast pain
Paleospinothalamic = associated with slow pain
Here possibly acute injuries let’s say bullet wound.
Initially, sharp pain. Also like thumbtack. Stimulating c
fiber for short periods of time can stimulate release of
glutamate and aspartate. For acute responses to painful
stimuli, glutamate ad aspartate will be released but in
this experiment c fibers also induce this release to
activate second order neuron in dorsal horn.
However, for chronic responses, for prolonged
stimulation of c fibers, other polypeptides like
substance P, cholecystokinin, g-related peptide,
neurokinin is co-released with glutamate and aspartate.
This is more complex than Guyton saying that: A delta
will be for glutamate and c fibers will be for substance P.
ALS which mediate your pain signals.
Referred Pain
o One well accepted theory now is the convergence
of afference from somatic structure and visceral
nociceptor which converges in the spinal cord
and since there is no cortical representation of
your viscera, most of the excitation of your
visceral receptors is reflected on various body
surfaces at the same dermatome as your visceral
receptors.
o For example, in cardiac pain, you would find it in
the inner aspect of left arm.
o When you have dysmenorrhea (assuming that
you are a female), do you experience referred
pain?
Projected Pain
o Phenomenon of projected pain which arises from
the so-called law of projection.
o In this law, when you excite a sensory pathway,
sensation generated will always be projected to
the site of the receptors for that particular
ascending pathway
o Eg. Ulnar nerve excitation: sensation projected to
fingertips.
o Phenomenon of projected pain can be used to
understand phantom pain.
PHYSIOLOGY: Neurophysiology of Somatic Sensations
Phantom Pain
o In phantom pain, (having phantom limb) pain is
arising from the body part which is
absent/amputated.
o Earlier hypothesis about phantom pain- even in
amputating it, severed nerve will regenerate.
There will be a kind of neuronal regeneration
which will contribute to hyperactivity of
regenerated axonal stump.
o The cortex will always project it to area of body
even if it is missing.
o What clinicians try to do is to inject with local
anaesthetics, sometimes they succed, but for
some, they don’t. Thus, phantom pain comes back.
o Dr. Ramachandran from india, a neurologist, found
out that many of his patients would report
phantom pain sensations on their upper arm.
Digits can be reflected in upper arm as well as in
face region. Follow-up studies in animals verify
same observations e.g. in monkeys.
Phanotom limb
o not necessarily pain, can merely be an
awareness that there still remains a certain part
of our body, even if it was already removed.
o animal studies: it can be due to cortical neurons
from the regions receiving activated synaptic
connections from adjacent regions of the body.
o Neuron 2 (the one once innervated by the
amputated limb) upregulates receptors, causing
denervation hypersensitivity
o Example, your forearm hand region receiving
sensory inputs from limb. Putol na yung sensory
signals, what could happen is that there are
axonal projections from adjacent regions e.g.
upper arm, face. Probably, there may still be
long term memories of amputated arm in
cortical neuron so that when upper arm or face
are activated, they activate also the cortical
neurons which were receiving signals originally
form the amputated region. This is the central
mechanism of phantom pain.
Cortical plasticity
Some functions of a cortical region will connect with
other cortical regions. If there is a sensory
deafferentation or cutting off of sensory signals, there
will be upregulation of synaptic receptors on the
postsynaptic neuron. If there are upregulation of these
receptors, they become sensitive to circulating
neurotransmitters which was described originally in
Phenomenon of denervation hypersensitivity.
Page 9
Withdrawal reflex
o generally sympathetic autonomic response
o There are some individuals who may report
opposite response.
o Generally, however, associated with
sympathetic response along with fight or flight
response.
o Slow pain, generally activated by c fiber
stimulation produce autonomic response
associated behavioral experiences like nausea
and thermoregulatory responses like profuse
sweating and deduction in muscle tone.
Rigidity
o We experience when visceral nociceptors are
activated e.g. appendicitis, diarrhea, dysentery,
severe stomach pain—doctors touch muscles,
rigid upon touch due to protective reflex.
o When visceral nociceptors are activated,
polysynaptic reflex can excite alpha motor
neurons in ventral horn which will activate
overlying muscles. This is a viscerosomatic
guarding reflex.
Chronic vs Acute pain
Chronic Pain Acute Pain
C fibers A delta fibers
How chronic pain works and how to manage it?
o it has been assumed that it will be passing
through ALS system
o thus, treatment may be via spinal cord
transsections focusing on anterolateral
quadrant.
o Mostly for patients with terminal cancer to
manage pain. Transecting ascending pathways
passing through ventral and lateral
spinothalamic tracts. They do transections of
anterolateral quadrant by surgery. They found
out that even surgery is not very successful for
chronic pain relief:
 there can be central structures,
supraspinal structures, above the
thalamus which become already
sensitive as a result of chronic pain
conditions or some types of chronic
denervations, or some reverberating
circuits.
 there can be some pathways which
can send collaterals through dorsal
column.
Guyton’s reverberating circuit theory—inputs will
cause action of higher reverberating circuit but what
present studies actually discovered is that synaptic
neurotransmitters can be upregulated in cases of
denervation causing activation of supraspinal pain
centers.
PHYSIOLOGY: Neurophysiology of Somatic Sensations
Itch and tickle
 usually innervated by C fibers
 a number are also activated by similar tissue
chemicals like histamine, kinine, elevated number
of bile cells, etc. and the same type of afferent C
fibers.
Clinical Correlations
Hyperalgesia = oversensitivity to noxious stimulus
Allodynia = pain caused by the non noxious movement
of sensitized skin e.g. boils on skin (when touched,
painful)
“Normally, when you touch skin, no pain. If you have a
pin and you touch it lightly on skin, it can sometimes
activate threshold of nociceptor and cause pain, but if
you do that to skin adjacent to a boil = very painful
hyperalgesia.”
Previously, noxious stimuli to normal skin can cause
more sensitive response to inflamed tissues. That’s a
hyperalgesic condition. In fact, there are discussions or
experimental conditions of primary and secondary
hyperalgesia.
o Secondary will be brought about by sensitization
of structures at spinal cord and above spinal
cord centers for pain processing.
o Primary it is only peripheral nerve endings that
are sensitized. Removal of the inflammatory
condition can result in absence of pain but in
secondary even removal of main source of
activation can still result in chronic pain
condition as result of sensitization of higher pain
order processing centers.
Hyperesthesia = oversensitivity to mechano and
thermoreceptive systems to non noxious stimulus
Hyperpathia = a pain syndrome characterized by an
increase in response with delayed onset, and an after
response that outlasts the stimulus; apparent after
repetitive stimulation
Hypoalgesia = undersensitivity to noxious stimulus
Hypoanaesthesia = undersensitivity to all
somatosensory modalities
*Anaesthesia relates to all somatosensory modalities,
even touch.
*Analgesia, just pain system. Complete congenital
absence of sensitivity to pain due to absence of A delta
and C fibers.
Complete Congenital Insensitivity = no C fibers&A delta
Causalgia and reflex sympathetic dystrophy = Part of
neuropathic pain-paindue to nerve injuries; upregulated
norepinephrine receptors
Page 10
Neuralgia = probably similar mechanisms
sympathetic dysreflexia; neuropathic pains
 Upregulation of norepinephrine receptors either
in soma or in regenerated axonal sprouts which
make them sensitive to circulating basal levels of
norepinephrine especially in times of stess. In
times of stress, fight or flight responses, higher
levels of serotonin which can excite nerve-injured
areas furthers.
 Closest biochemical model for reverberating
circuit of Dr. ganong: but this one is brought
about by glutamate so there is no such circuit of a
circle/pathway of nerves whch have been found
experimentally but only expt’l evidence is
pathways (pain pathways) which releases
glutamates as well as polypeptides like substance
Postsynaptic neuron and induces release of nitric
oxide which further excites presynaptic neuron.
to  There are conditions of plasticity
in learning. Learning itself is a
good model of plasticity.
 When we learn/remember there
are structural changes happening
in our brain. In order for us to
remember something/be good at
something, we have to do
repetitive stimulation (Repetitive
stimuli of certain pathway) and
Some emotional affective
components (you feel well-
motivated), emotional cues. At
the same time, there are
emotional deterrents to further
learning e.g. stress.

 Nitric oxide, for example, has been known to

diffuse to the presynaptic neuron in central
pathways causing positive feedback mechanism-
hyperexcitation of this pathway.

Plasticity
 in normal conditions, may not happen but with
hyperactivation of pathway due to injury to nerve,
it can be possible
 Eg. Normally, nitric oxide is not produced much
but with hyperactivation of this pathway, nitric
oxide is formed and would lead to positive
feedback of the mechanism.
 Another example of plasticity would be
regeneration of adjacent neurons in phantom
pain. Causes us sensation of a limb which has
been cut off as though it is present.
 Other examples- you’re blind so your visual
cortex is not well used but your somatosensory
neurons from anterior parietal and posterior
clacarine cortex would be possibly invading (in
terms of synaptic connections to your visual
cortex). Possibly, visual cortical neurons now will
be having synaptic connections with
somatosensory cortex in performing work very
similar to somatosensory neurons.
 Normally, ganito specialized functions niya pero
due to changes in environment, they perform
either functions.
o For example, left brain, right brainfor
young people, infants, with brain
damage, left hemisphere is destroyed
(language-specialized), right hemisphere
still intact, language functions can still be
developed in left hemisphere because
right hemisphere takes over such
functions.
 Such plasticity gradually decrease
when we’re older.

PHYSIOLOGY: Neurophysiology of Somatic Sensations Page 11

  Aβ = large, myelinated, group2
 Small receptive field =accurate in
localizing stimulus source
 Large receptive field = not accurate in
localizing stimulus source

Characteristic Pacinian Meissner’s Merkel’s Ruffini’s Ending Hair Follicle

Corpuscle Corpuscle Disk Endings

code FA-II FA-I SA-I SA-II FA-I??

Adaptation Fast Fast Slow Slow Fast

Receptive field size large small small large small

Touch, vibration speed of stimulus localization of magnitude and Light touch
Encoded Sensation (acceleration application, low stimulus (touch duration of flutter; low
detector) freq vibration pressure) stimulus (touch vibration sensors
sensors (like pressure); (30-40 Hz, like
pacinian, though because it is Meissner’s)
meissner’s have slowly adapting,
lower sensibility: it can give
30-40Hz) accurate
description
magnitude and
duration… unlike
those that are
rapidly adapting
generally Aβ Aβ
Afferents (with some Aα) Aβ Aβ (with some Aα) Aβ

fingertips, lips, high density in ??

Location Skin skin, even at fingertips, lips, covered by liquid
sexual erectile many skin areas filled collagen
tissues, glans
penis, etc.
Onion like
Notes / Remarks lamellar capsule

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PHYSIOLOGY: Neurophysiology of Somatic Sensations Page 13