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L4, Somatic sensation and physiology of pain - physiology

  Somatic sensation and physiology of pain

 Lecture video

:Data link

https://n9.cl/gumc93

Classification based on the site of Receptor

A) Superficial (Exteroceptive) sensations;

Resulting from stimulation of receptors in the skin, e.g.

Pain
Touch
Temperature

Deep(Proceptive)sensations

Resulting from stimulation of receptors in structures deep to the skin as
A) Spinothalamic sensations; Passes through the spinothalamic tracts
1- Pain
2-Tempreture
Passes through the lateral spinothalamic tract
3. Crude touch passes through the ventral spinothalamic tract.
B) Dorsal column sensations:
Passes through the dorsal column tracts (gracile & cuneate tracts) for fine touch and
all deep sensation

Classification based on the CENTER of perception

Protopathic (Crude) sensations

Can be perceived in the thalamus

. Slow pain.
. Extreme grades of temperature
. Crude touch

B)Epicritic(Fine)Sensations

Cortex is their sensory center
Fast pain
Fine grades of temperature
Fine touch
Deep sensation

PAIN

Definition

It is unpleasant sensation resulting from tissue damage. However, it is a protective sensation.
RECEPTORS:

Nature: Free nerve endings.
Distribution:
Widespread in superficial layers of the skin, periosteum, arterial wall, joint surfaces, dura of falx and tentorium cerebri.
- Poorly present in most other deep tissues.
Not present in brain substances and parenchymal tissues of the liver, kidney, and lungs (they are pain insensitive structures).

Types

o Mechanosensitive pain receptors


Thermosensitive pain receptors
- Stimulated by thermal damage to the tissues, e.g., extremes of heat (above 45°C) or cold (belo 10°C).
Mainly distributed in the skin.


Dull aching pain: more diffuse, come from deep tissues.

 Throbbing pain: fluctuating in intensity, results from localized inflammation in deep tissues,
 e.g., an abscess

 Mechanism of stimulation

 Stimulated by tissue damage.

 Tissue damage releases certain substances, e.g., histamine, serotonin, bradykinin, prostaglandin, acids, excess K+. These substances stimulate pain receptors.

 Adaptation:

  • Pain receptors are slowly adapting.

According to site of origin

) Cutaneous pain

Origin: Arises from skin and subcutaneous tissues.

 Character (nature): pricking or burning.

Afferents: A-delta or C-fibers. - Types: Fast or slow.

Localization: well localized compared with other types of pain



Associated changes

Somatic changes: withdrawal reflex.

Autonomic reactions:

 Mild and moderate pain sympathetic stimulation → Heart rate and arterial blood pressure

▪️ Severe pain → parasympathetic stimulation - H.R. and ABP.

 Emotional reactions in the form of anxiety, fear, crying, depression.

Causes: any form of painful stimuli, e.g., mechanical, thermal, chemical,
Types of cutaneous pain

 

Deep pain


Origin: Arises from structures deep to the skin, e.g., muscles, joints, tendons, ligaments, and periosteum.

Character (nature): usually dull aching.

Afferents: non-myelinated C-fibers.
Types: Only slow.

Localization: poorly localized.

Associated changes:

 Somatic changes: in the form of spam of the overlying skeletal muscles.

2) Autonomic reactions: in the form of ↓ H.R. and ABP.

Causes: Ischemia (1 blood flow) to skeletal muscle, e.g. due to spasm which leads to:

  1. 1. Damage of muscle fibers and liberation of bradykinins and other substances.
  2. 2. Accumulation of metabolites, e.g. lactic acid.
  3.  Both 1 & 2 stimulation of pain receptors.

Visceral pain

Origin: Arises from internal viscera.
  •  Character (nature): dull aching, or colicky.

  • - Afferents: non-myelinated C-fibers which pass mainly with autonomic nerves [sympathetic and parasympathetic].

  • - Types: Only slow

  • - Localization: poorly localized.

  • - Associated changes:

Somatic changes: in the form of spam of the overlying skeletal muscles.

Autonomic reactions: in the form of ↓ H.R. and ABP.

Emotional reactions in the form of anxiety, fear, crying, depression

REFERRED PAIN

DEFINITION
Pain felt away from site of its origin. Visceral pain is not felt at the diseased viscus but felt at the skin area supplied by the same dorsal root.

EXAMPLES

  1. Cardiac pain is referred to the base of the neck and left shoulder.
  2. Gall bladder pain is referred to the right shoulder.
  3. Pain from the appendix is referred to the skin around the umbilicus.
  4. Renal and ureteric pain is referred to the upper part of the thigh and testicles.

MECHANISM


1) CONVERGENCE PROJECTION THEORY:

▪️ Afferent pain fibers from the skin area and diseased viscera converge on the same second order neuron and finally stimulate the same cortical neuron. Cortex will project pain to skin (feel pain as if it is coming from the skin) because the sensory cortex is accustomed to receive pain from the skin [the skin is the commonest site of pain]. Convergence may also occur at thalamus or sensory cortex.

FACILITATION THEORY


 Visceral pain afferent sends a collateral branch to facilitate the second order neuron of pain pathway from skin area of reference facilitation of - pain sensation from the skin area, i.e., minor activity in the pain pathway from skin area →pain sensation.

▪️ Evidence: Local anesthesia of the area of reference sometimes abolishes or decreases referred pain. Thus, convergence and facilitation play a role in pathogenesis of referred pain.

Note: Dorsal horns are divided on the basis of their histological characteristics into 6 laminae, from lamina I [Lamina marginalis] to lamina VI. Neurons in laminae II and III are substantia Gelantinosa of Rolandi (SGR)

PATHWAY OF PAIN


A. Pathway of FAST PAIN: Composed of 3 neurons 1) First order neuron (Dorsal root
ganglion}

Receptors: Free nerve endings

Afferent: A-delta fibers

End around neurons in lamina I in dorsal horn of the spinal cord

Second order neuron (Cells in lamina I of dorsal horn}: Axons of the cells of the second
order neuron:

Cross to the opposite side in front of the central canal then
Ascend to form -Lateral spinothalamic tract in the spinal cord (neospinothalamic tract)

-Spinal lemniscus in the brain stem

End around posteroventral nucleus of the thalamus

3) Third order neuron (Postero-ventral nucleus of thalamus): Axons ascend to pass through the posterior limb of internal capsule to reach the somatic sensory areas


Notes: 1-Few fibers of the neospinothalamic T terminate in reticular formation

Pathway of SLOW PAIN

1) First order neuron (Dorsal root ganglion}:

Receptors: Free nerve endings.

Afferent: C-fibers.

End around neurons in lamina II and III (Substantia gelatinosa of Rolandi, SGR).


2) Second order neuron (SGR in lamina II and III}:

Axons cross to the opposite side in front of the central canal of the spinal cord and ascend to form the lateral spinothalamic (Paleo-spinothalamic tract in the spinal cord. End around neurons in the reticular formation (mainly) and non-specific nuclei of thalamus (intralaminar and midline nuclei) of the thalamus (only few fibers)

3) Third order neuron:

Fibers arise from the reticular nuclei and non-specific thalamic nuclei ascend in the sensory radiation and terminate diffusely in all areas of the cerebral cortex


Note: excitatory chemical transmitter "substance P" is the chemical transmitter released at the central end of the C-fibers that carry slow pain.




PAIN CONTROL SYSTEM
(Endogenous analgesic system)

It is a system by which pain is inhibited. It is composed of 2 systems:

1. Supraspinal (Brain's) system

 In this system stimulus for pain inhibition starts from supraspinal centers, which are opioid receptors and passes through 3 neurons to inhibit the pain afferent

1. Opioid receptors:

Opioid receptors are present in:

a. Periventricular area: around the third ventricle.

b. Periaqueductal area: around the aqueduct of Sylvius in midbrain and pons.



Opoid Receptors

Opioid receptors are stimulated by opioids [opioid peptides) that may be 


Exogenous: morphine and related compounds

Endogenous, e.g., endorphins present in hypothalamus and pituitary gland and released to blood during stress [acts as neurohormones]. This explains stress analgesia

These opioid receptors send enkephalinergic fibers to raphe nucleus present in lower pons and upper medulla

 Raphe magnus nucleus: sends serotonergic fibers [serotonin secreting neurons] through the dorsal aspect of lateral column of the spinal cord to interneurons in the dorsal horn of the spinal cord

3. Interneurons in the spinal cord: They inhibit the release of the chemical transmitter from the pain afferent (C and A-delta fibers), thus inhibiting pain transmission [presynaptic inhibition mainly but postsynaptic may have a role]. These interneurons are enkephalinergic

Spinal (Spinal inhibition) system

A-beta fibers inhibition (Inhibition by touch fibers]

Stimulation of A-beta fibers of], thus pain sensation is inhibited.

This mechanism also explains why liniments are oftouch, e.g., rubbing the skin around a painful area, inhibits pain sensation.

Mechanism: touch fibers send collaterals that end on central termination of C-fibers for pain. These collaterals prevent the release of the chemical transmitter [Substance P] from C-fibers [presynaptic inhibitionten useful for pain relief.

Mechanism of acupuncture for relief of pain is probably by this mechanism together with simultaneous psychogenic excitation of the central analgesia system


Gate theory of pain

The cells of substantia gelatinosa of Rolandi of the cord acts as a gate through which pain impulses reach the lateral spinothalamic tract. This gate may be closed by

Impulses descending in dorsolateral column of the spinal cord

Impulses along collaterals from A-beta fibers for touch

 Impulses along collaterals from A-delta fibers for pricking pain.

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