PHYSIO B GENERAL SENSES 2

FEU-NRMF Institute of Medicine

Lecturer: Felipe Barbon, MD 2.5.14 1B-Medicine 2017

GENERAL OR SOMATIC SENSE These sensations will depend on type of environment the
- Involves activation of receptors present in all parts of the person is used to.
body TEMPERATURE THERMAL SENSATION
0 10 C Pain
TYPES OF SOMATIC SENSE: 10 15 C Pain / Cold
15 25 C Cold
1. MECHANORECEPTIVE SOMATIC SENSE 25 36 C Cold/ Warm
- Utilize receptors with low threshold (sensitive) receptors 36 37 C Indifferent sensation
- Sensitive to mechanical stimulation: (body temp)
Touch > 37C Hot
Pressure > 40C Pain
Vibration (Pallesthesia)
Tickle & itch 3. NOCICEPTIVE SOMATIC SENSE
Position/ Proprioceptive sense - Utilizes both high & low threshold receptors
o Static position sense: ability to know position of a - 3 types:
non-moving body part in relation to environment Mechanosensitive nociceptors
o Dynamic position sense (Kinesthesia): ability to ~ Uses type A delta neurons = fast/acute pain
know which nody part is moving along with the ~ pain is due to excessive mechanical movement of
direction & range of movement body part (e.g. too much bending or stretching)
- E.g: Pacinian corpuscles, Merkels disc, Meissners Thermosensitive nociceptors
corpuscles, etc ~ Uses type A delta & type C neurons = dual sense
~ Pain due to extreme temperatures
2. THERMORECEPTOVE SOMATIC SENSE
- utilize high threshold receptors Chemosensitive nociceptors
- sensitive to thermal changes ~ uses type C neurons = slow/chronic pain
- classified into 3 groups: ~ pain due to receptor release of chemical agents in
Cold sensitive thermoreceptors response to tissue damage
~ Greater number in body ~ these chemical agents are known as P-factors or
~ Has DUAL SENSE: uses type A delta & type c neurons Pain-causing factors
(you have an acute sense followed by a delayed P-Factors (Pain-causing factors)
sense) - released every time there is tissue damage
~ Activated at 25C body temp
- release of these agents, esp. in excess, can cause pain
Warm sensitive thermoreceptors by stimulating chemosensitive nociceptors
~ Fewer in number - release can also increase sensitivity of other types of
~ Uses type C neurons (delayed or chronic sensation)
nociceptors by decreasing their stimulation threshold
~ Activated at 44C body temp
this is why when there is tissue injury, slight movement of
Pain sensitive thermoreceptors the body part already causes pain because
~ Once stimulated can cause pain mechanocceptors are altered
~ Also has dual sense: uses type A delta & type C example: tissue injury in hand, slight movement of fingers
will cause additional pain
neurons
- some directly affect/stimulate chemosensitive
~ Stimulated at temp < 15C and >40C
nociceptors & some do not directly affect the
*Adaptation:
chemosensitive nociceptors but enhance pain by
cold sensitive & warm sensitive thermoreceptors are
capable of adapting, at a range between 20C-40C increasing sensitivity of nociceptors/pain endings to
pain sensitive thermoreceptors ARE NOT capable of different P-factors
adapting Agents that directly affect chemosensitive nociceptors:
Bradykinin most effective
The Principle of Body Heat Loss & Gain: Serotonin
To have thermal sense, you have to have a TRANSFER OF Histamine
HEAT ENERGY CCK
Cold sensation: heat lost to the cooler object Acids: Lactic acid responsible for anoxic pain
Warm sensation: heat gained from hot object Acetylcholine
Indifferent sensation: there is no heat transfer (equal Proteases
stimulation of cold sensitive & warm sensitive Hydrogen & Potassium ions
thermoreceptors)

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PHYSIO B GENERAL SENSES 2
FEU-NRMF Institute of Medicine
Lecturer: Felipe Barbon, MD 2.5.14
Agents that increase nociceptor sensitivity to P-factors:
(In some books called Tachykinins)
Prostaglandin: blocked by ASA (acetyl salicylic
acid/aspirin)
Substance P: blocked by opioids
Calcitonin gene related peptide (CGRP)
- enhances activity & release of Substance P
- inhibits the enzyme that degrades Substance P,
prolonging its stay in the area enhanced activity of
P-factors enhanced sensitivity of nociceptors
Mechanism of action of Opiods for pain management:
Inhibits Substance P
decrease Ca influx, decreasing AP generation duration of
nociceptors
decrease sensitivity of dorsal horn by hyperpolarizing its
membrane (this is why other sensations are also inhibited in
opioid use)
3 Major Sites where Opiods has an effect:
1. Site of injury/ tissue damage = effect is local anesthesia
2. Dorsal horn
3. Brainstem = effect is general anesthesia
*can also affect thalamus where most pain pathway passes
Upon injury, you release the P-factors: Bradykinin, 5HT (Serotonin),
Histamine & Prostaglandins
Release of Substance P is enhanced by CGRP
REVIEW ON BLOOD:
Agents released by platelets on blood vessel injury: 5HT, TXA2 & ADP
- 5HT can stimulate pain receptors & cause vasoconstriction
- TXA2 derived from prostaglandins enhance activity of platelets to
move towards site of injury
- ADP enhances stickiness of platelets enabling them to form a
plug
DISTRIBUTION OF PAIN RECEPTORS:
- types of tissues with numerous pain receptors are usually
coverings: skin, periosteum (bone covering), arterial walls,
joints, pleura (lung covering) & cranial vault: falx &
tentorium (brain coverings)
brain itself & bone matrix has no receptors, they are present in
their coverings
2nd degree burn is more painful than 3rd degree burn because the
free nerve endings are already destroyed
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1B-Medicine 2017
Cont. Distribution of Pain receptors:
pin prick & getting blood from arteries is more painful than
venipunctures
a person will not notice TB infection because it initially destroys
the parenchyma so there is no pain; pain only starts when the
bacteria already reached the pleura causing pleuritis
- it is located in such manner (coverings of vital
organs/tissues) for immediate protection of these
structures, now preventing further damage
Purpose of pain is for protection: mimic painful body part to
facilitate healing & rest of the body part for recovery
CLASSIFICATION OF A PERSON AS TO PAIN SENSITIVITY:
1. Hyperpathia (Pain insensitive)
2. Hyperalgesia (Pain sensitive, exaggerated reaction)
Primary: problem is on region where you have the
receptors (skin)
Secondary: problem is on the pain pathways (spinal
cord, brainstem)
- Allodynia (supersensitive)
~ type of a primary hyperalgesia
~ even minor stimuli that cannot cause pain on normal
persons can cause these individuals pain
~ sensitization of silent nociceptors: even non-active
receptors are eventually activated due to change in
condition of site of receptor
~ example: sunburn (altered skin) - even slight touch on
skin can cause pain
NEUROPATHIC PAIN
- pain even in the absence of nociceptor stimulation due to
damage to neurons involved in transmitting pain impulses
- pain is caused by stimulation of afferent sensory neurons
- examples: causalgia & phantom-limb pain or projected
pain (pain on amputated limb)
CENTRAL PAIN
- injury involving the thalamus (center for chronic pain) or
at any level of the spinothalamic tract
- usually severe & spontaneous
- example: men with thick wallets in the back pocket causes
compression of the sciatic nerve
PHYSIO B GENERAL SENSES 2
FEU-NRMF Institute of Medicine
Lecturer: Felipe Barbon, MD 2.5.14 1B-Medicine 2017

2 PAIN PATHWAYS: PAIN SENSATIONS

- Classified into:
1. ACUTE FAST (1st) PAIN PATHWAY Skin/Superficial Pain
- Also called the Neospinothalamic Tract Projected Pain or Phantom-limb Pain
- Use type A delta neurons Visceral/Deep Pain: injury is present in the visceral
- Once activated can enter the dorsal horn & transmit tissues (ex. Kidney stones)
impulses using the spinothalamic tract towards the Referred Pain
center --- it can go up to the parietal lobe where the
somatic sensory area is located REFERRED PAIN
- Easier to localize (Epipritic pain/senses): because they - Injury is present in the visceral tissue but perception of
can reach the sensory homunculus pain is in the superficial or somatic tissue
- Passes at lamina I and V (mostly Lamina I & some books - Example:
say it can also use Lamina X) Initial period of ischemia pain in left shoulder
- Major Neurotransmitter Agent (NTA): mostly Initial period of appendicitis pain in epigastric are
Glutamate, sometimes Substance P Initial kidney injury pain in upper thighs
- Impulses reaches the ventrobasal complex and - most referred pains eventually become visceral pain
posterior nuclear group of the thalamus chronic ischemia manifests as chest pain
appendicitis eventually manifests lower quadrant
pain
- referred pain happens because:
somatic & visceral impulses have the same entry
point upon on the spinal cord
convergence of neurons are observed on the
second order neuron (Convergence-projection
Theory)
*initially, cortex
becomes confused
where the impulses
are coming from,
but upon
Activation Dorsal Horn Spinothalamic tract Center
aggravation of
injury it becomes
2. CHRONIC SLOW (2nd) PAIN PATHWAY
clear that the
- Also called the Paleospinothalamic Tract
visceral organ is the
- Use type C neurons, some use type A delta
one damaged
- Once activated transmission of impulses is same with
the acute pathway but it usually stops at the thalamus
- Center is the thalamus
where majority of impulses are analyzed
If ever transmission reaches the cortex, they will not
go the parietal lobe (somatic sensory area) instead, it
will go to the frontal lobe & limbic system creating
now emotional pain
Thats why chronic or lingering pain is also called
thalamic pain
Hard to localize (protopathic pain/senses): cannot
reach sensory homunculus
- Passes at lamina II and III
- Major NTA: mostly Substance P but sometimes
glutamate also
- Impulses reach the reticular formation, some enter the
intralaminar nuclei of the thalamus

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PHYSIO B GENERAL SENSES 2
FEU-NRMF Institute of Medicine
Lecturer: Felipe Barbon, MD 2.5.14
PAIN SENSATIONS
- always associated with changes with the activity of the
ANS, especially chronic pain
- pain perception decreases whenever there is
simultaneous activation of other somatic receptors
reason why massaging/applying pressure on temples
relieves headache (brain now listens to impulses
coming from pressure receptors & ignore nociceptors)
PAIN SUPPRESSION/INHIBITION
- pain insensitive persons do not feel pain because they can
effectively suppress pain via activity of Gating Neurons &
the Analgesia System
ANALGESIA SYSTEM
- Location:
Brainstem:
~ periaqueductal gray area in midbrain & upper pons
~ raphe magnus nucleus in the lower pons & upper
medulla
Spinal cord: pain inhibitory complex in the dorsal horn
- needs development to resist pain, but when activated it
will have longer effect
- constant subjection to pain will eventually
develop/activate analgesia system
*athletes & soldiers have greater pain tolerance because this
- NTA used to suppress activity of pain sensory fibers:
Enkephalins (related to Morphine)
- Enkephalin secreting neurons
Release enkephalins
Activity is enhanced by the presence of Serotonin &
Norepinephrine
Present up to the brainstem
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1B-Medicine 2017
GATING NEURONS
- present in the substancia gelatinosa (Lamina II) of the
spinal cord
- involved in stress-induced analgesia due to increased
cortical activity
- instantly activated when needed by a person but ability to
resist pain lasts only for a short period
- NTAs: GABA & Glycine
- Increased cortical activity: activated gating neurons
closed Lamina II (act as gates) no pain sensation
- Decreased cortical activity: stop activity of gating neurons
open Lamina II
PURPOSE OF PAIN
- For protection: informs center that a certain area is
injured
- Warning/threat
- Allows/Forces body to rest by limiting movement
- Basis for learning: an individual adapts to avoid same
painful stimulus if it occurs again
SENSORY ASCENDING PATHWAYS
DORSAL COLUMN/MEDIAL LEMINISCUS PATHWAY
- Transmission of discriminative sensations: fine touch, fine
pressure, vibrations & proprioception
- Limited to mechanical sensations
- Testing for Integrity of Dorsal Column:
Gracilis pathway: test mechanical abilities of lower ex
Cuneatus pathway: upper ex
- Tests for integrity by using discriminative tests such as:
Fine touch (stereognosis, graphestesia, 2-point
discrimination)
Proprioception
ANTEROLATERAL/SPINOTHALAMICPATHWAY
- Transmission of pain & thermal sensations
- also for non-discriminative sensations: crude touch &
crude pressure, tickling & pleasurable sensations
- broad spectrum: not limited to mechanical senses
- Test for integrity:
Inflict pain
Thermal sensations
Pleasurable sensations
SENSATIONS OF THE FACE
- Innervated by CN V (trigeminal nerve) divided into three
divisions (ophthalmic, maxillary and mandibular divisions)
- Back of the head is innervated by cervical spines (C2)
PHYSIO B GENERAL SENSES 2
FEU-NRMF Institute of Medicine
Lecturer: Felipe Barbon, MD 2.5.14 1B-Medicine 2017

ANTERIOR SPINAL ARTERY OCCLUSION

- Damage to ventral portion of spinal cord leads to motor
deficits and spinothalamic sensations
- Problem due to occluded blood flow (compression)

COMPLETE CORD TRANSECTION

- Permanent paraplegia full paralysis of lower body
- Paralysis below the level of injury
- Autonomic problems
- Loss of sensory & motor functions
- Spinal shock (loss of spinal reflexes): presence of
autonomic, sensory & motor problems

DESTRUCTION OF SOMESTHETIC CORTEX

- Cortex: involved in the analysis of all somatic impulses
(particularly the parietal lobe)
Loss of ascending tract functions
Atopognosis
Astereognosis
Amorphosynthesis: patient ignores contralateral side of the
body
Inability to judge critical degrees of pressure sensation
Inability to determine body position
CLINICAL CONDITIONS:
Inability to approximate weight of an object
Poor localization of pain/thermal sensations
BROWN-SEQUARD SYNDROME - Complete anesthesia in cortical (parietal lobe) injury is
- Lateral hemisection of the spinal cord rare : Chronic pain is always retained due to intact
- Due to trauma, tumor or ischemia to certain parts of thalamus
spinal cord - Contralateral manifestations
- Common in gunshot wounds - TO DETERMINE SEVERITY OF DAMAGE :
- Dorsal column damage: Ipsilateral loss of proprioceptive,
vibratory and discriminative sensations
SENSATIONS 1st TO
- Spinothalamic damage: Contralateral loss of pain &
DISAPPEAR
thermal sensations MILD Fine touch
- Corticospinal/Motor tract: Ipsilateral paralysis
MILD MODERATE Proprioception
- Manifestations in 1 or 2 segment lower than lesions
MODERATE SEVERE Thermal sensation
SEVERE Acute pain sensation
TABES DORSALIS
- Damage to the dorsal roots & columns
UPON RECOVERY SENSATIONS 1st TO
- Impairment of proprioception and vibratory sensations
- Positive Rombergs sign abnormal proprioceptive REAPPEAR
*last to disappear is Pain
- sense
first to reappear Thermal sensation
- Anterolateral system functions are left intact
- Loss of deep tendon reflexes Proprioception
Fine touch (fully recovered)
SYRINGOMYELIA
- Central lesion of the spinal cord affecting the decussating
fibers of the spinothalamic tract
- Segmental loss of pain and thermal sensation (bilateral)
- Spared dorsal column: Normal touch, pressure, vibration
and proprioception
- Severe damage results to cape-like distribution of the
abnormality in the upper thoracic area and upper
extremities