/
 Pain  Pain is an unpleasant sensation which is a primarily protective mechanism that  Pain  Pain is an unpleasant sensation which is a primarily protective mechanism that

Pain Pain is an unpleasant sensation which is a primarily protective mechanism that - PowerPoint Presentation

phoebe-click
phoebe-click . @phoebe-click
Follow
343 views
Uploaded On 2020-04-03

Pain Pain is an unpleasant sensation which is a primarily protective mechanism that - PPT Presentation

T he sensation of pain is accompanied by motivated behavioral responses such as withdrawal or defense as well as emotional reactions such as crying or fear Also unlike other sensations the subjective ID: 775203

pain fibers amp area pain fibers amp area system tract spinal pathway receptors spinothalamic cortex dorsal neurons sensory cord

Share:

Link:

Embed:

Download Presentation from below link

Download Presentation The PPT/PDF document " Pain Pain is an unpleasant sensation w..." is the property of its rightful owner. Permission is granted to download and print the materials on this web site for personal, non-commercial use only, and to display it on your personal computer provided you do not modify the materials and that you retain all copyright notices contained in the materials. By downloading content from our website, you accept the terms of this agreement.


Presentation Transcript

Slide1

Pain

Pain is an unpleasant sensation which is a primarily protective mechanism that is meant to bring to conscious awareness that tissue damage is occurring or is about to occur.

Slide2

T

he

sensation of pain

is accompanied

by motivated behavioral responses (such as

withdrawal or

defense) as well as emotional reactions (such as

crying or

fear

).

Also, unlike other sensations, the subjective

perception of

pain can be

influenced

by other past or

present experiences

(for example, heightened pain perception

accompanying fear of the dentist or lowered pain perception in an injured athlete during a competitive event).

Pain is detected by pain receptors also called “

Nociceptors

”.

Pain is said to be a sensation and an emotion.

Adaptation to pain is poor.

Pain receptors are specific for Pain but not for the stimulus.

COMPONENTS OF PAIN:

Nociception:

the body’s detection and signaling of noxious events.

Pain:

the conscious perception or recognition of the nociceptive stimulus, and

Suffering:

the individual’s reaction to pain with emotional, somatic and autonomic effects along with efforts to avoid or escape pain. (This reaction differs from person to person & is influenced by age, sex, culture and personality; the reaction is also affected by the intensity & duration of pain.)

Slide3

TYPES OF PAIN

SHARP PAIN

Also called Physiologic pain. Quick in onset.Felt within 0.1 sec if a pain stimulus is applied. Sharp & pricking. Also categorized as acute pain & electric pain. Well localized. It is not felt in many deeper tissues of the body. E.g. needle puncturing the skin, knife cutting a skin, burn. Conducted by A-delta fibers.

DULL PAIN

Also called Pathologic pain or chronic pain. It includes inflammatory and neuropathic pain.

Slower in onset.

Starts after 1 second of application and increases slowly over many seconds & sometimes minutes.

Greater duration and less localized. It can lead to almost prolonged and unbearable suffering.

It is associated with tissue destruction.

Dull, aching pain, slow pain, throbbing pain, nauseous pain.

It can occur in skin and deeper tissues.

Conducted by C type fibers.

Slide4

Pain Receptors & their Stimulation

The pain receptors in the skin and other tissues are all free nerve endings.

They

are widespread

in:

-

superficial

layers of the

skin.

-

certain

internal tissues

, such as the

periosteum

,

the

arterial

walls,

the

joint

surfaces

,

and the

falx

and

tentorium

in

the cranial

vault.

-

Deeper

tissues

are only sparsely supplied

with

pain

endings.

Pain can be elicited by multiple types of stimuli. They are classified

as:

M

echanical

,

T

hermal

,

and

Chemical

pain stimuli

.

In general, fast pain is elicited by the mechanical and thermal types of stimuli, whereas slow pain can be elicited by all three

types.

Pain receptors DO NOT ADAPT AT ALL or if they do, very little.

Slide5

Mechanism of pain production

Tissue Damage

Tissue Ischemia

Chemical substances

Muscle spasm

Slide6

1. Tissue Damage

Slide7

2. Tissue Ischemia

When a tissue does not receive the required amount of blood supply, it becomes painful in a very short time, it becomes painful in a vey short time.

Thus, if the blood supply is stopped to the upper limb by applying a tourniquet, pain appears within 3-5 minutes. If the forearm of the same limb is forced to exercise, the pain appears within 15-20 seconds.

Myocardial ischemia, Angina Pectoris and intermittent claudication are examples of pain due to tissue ischemia.

Slide8

Mechanism of Pain production (cont.)

3. Chemical Substances

Some chemicals that excite the chemical type of pain: Bradykinin Histamine SerotoninAcetylcholine Potassium ionsProteolytic enzymes. Some chemicals like Substance P and Prostaglandins enhance the sensitivity of pain endings but do not excite them directly. Other chemicals may get deposited in different tissues of the body and cause pain, such as urates depositing in the synovial membranes of joints leading to gouty arthritis which is a very painful condition.

4. Muscle Spasm

When muscle spasm, the blood supply is decreased leading to decrease in oxygen supply, increased metabolites collecting at the site leading to pain.

The contracted muscle compresses its own blood vessels leading to more ischemia and more pain.

This sets up a vicious cycle or a positive

feedback cycle.

Slide9

ASCENDING PATHWAYS

Slide10

ASCENDING PATHWAYS

Three-neuron pathways:Primary sensory neurons: - From external receptors - Travel through dorsal roots of spinal cordSecondary neurons: - Make up tracts in spinal cord and brainstemTertiary neurons: - From thalamus to primary sensory cortex - Travel through internal capsule

For conscious perception:

Spinothalamic

system

Medial

Lemniscal

system

For unconscious perception:

Spinocerebellar

Spino-olivary

Spinotectal

Spinoreticular

Slide11

ANTEROLATERAL SYSTEM

Anterior

Spinothalamic

Pathway:

Crude touch, itch, tickle & pressure

Lateral

Spinothalamic

Pathway:

Pain & temperature

Slide12

The Anterolateral system is made up

of:

Anterior

Spinothalamic

Pathway

Lateral

Spinothalamic

Pathway

The anterior

spinothalamic

tract carries fibers for crude touch, tickle, itch and pressure while lateral

spinothalamic

carries fibers for pain and temperature.

There is a double system of pain innervation in the Lateral

Spinothalamic

tract:

NEOSPINOTHALAMIC PATHWAY: For FAST pain carried by A-delta fibers

PALEOSPINOTHALAMIC PATHWAY: For Slow pain carried by C fibers.

Because

of this double system of pain innervation, a sudden painful stimulus often gives a "double" pain sensation: a

fast-sharp (also called

First

pain)

that is transmitted to the brain by the

fibers,

followed a second or so later by a

slow (Second pain)

that is transmitted by the C

fibers.

The A-delta and C fibers carrying pain & temperature information from the body terminates in the dorsal horn of the spinal cord.

- A-delta fibers terminate in lamina I, V and X (Lamina

marginalis

of the gray matter)

- C fibers terminate in lamina I and II (

substantia

gelatinosa

of the gray matter)

The distinct termination patterns of A-delta and C fibers in the spinal cord suggest that the messages are kept separate so that feel two distinct types of pain.

The primary afferent fibers for pain in the head enter the brainstem through the trigeminal nerve. The trigeminal distribution includes fibers for both the head and toothache pain.

Glutamate is the NT for the pathway for Fast pain while Substance P is the NT for the pathway for Slow pain.

Slide13

Anterior & LATERAL SPINOTHALAMIC TRACT

Even though all pain receptors are free nerve endings, these endings use two separate pathways for transmitting pain signals into the central nervous system. The two pathways mainly correspond to the two types of pain-a

fast-sharp pain pathway

and a

slow-chronic pain

pathway.

Slide14

Receptors (Mechanoreceptors, Thermal & Pain receptors)

Fast

Pain carried by A-delta fibers (6-30 m/sec)

Slow

Pain carried by Type C fibers (0.5-2 m/sec)

First Order Neuron

Posterior root ganglion (Cell bodies)

Fibers ascend or descend 1-2 spinal cord segments where they are called the

Tracts of

Lissaeur

On entering the spinal cord, the pain signals take one of the two pathways:

Neospinothalamic

pathway ---

Paleospinothalamic

pathway

Lamina I of dorsal horn

Lamina II & III of dorsal horn

(Lamina

marginalis

) (

Substantia

Gelatinosa

)

↓ ↓

Second order neurons Second order neurons

↓ ↓

Decussate immediately through the anterior commissure & then ascend in the anterior & lateral columns of the opposite side of the spinal cord.

Slide15

Ascend through the brainstem (medulla, pons & midbrain)as the Spinal Lemniscus (where fibers of Anterior & Lateral Spinothalamic tract ascend together in the lower part of medulla)↓ Thalamus (VPL nucleus) Some fibers carrying the slow pain also relay to the Reticular area, Tectal area and Periacquiductal gray region giving rise to SPINOTECTAL and SPINORETICULAR tract ↓ Third Order neurons ↓ Somatosensory Cortex(Some fibers carrying the fibers for slow pain also terminate in the hypothalamus)

Slide16

THE ANTEROLATERAL PATHWAY

Slide17

Slide18

Why you CANNOT sleep when you are in pain?

Electrical stimulation in the

reticular areas of the brain stem

and in the

intralaminar

nuclei of the thalamus,

the areas where the slow-suffering type of pain terminates, has a strong arousal effect on nervous activity throughout the entire brain. In fact, these two areas constitute part of the brain's principal "arousal

system." This explains

why it is almost impossible for a person to sleep when he or she is in severe pain.

Slide19

What can be done when a person is suffering from intractable and severe pain?

Slide20

Effect of Lesion

Anterior

Spinothalamic

Tract:

The destruction of this tract produces little if any tactile disturbances as touch is also carried in DCML.

Bilateral lesion of this tract leads to loss of sensations of crude touch, itch and tickle below the lesion.

The unilateral lesion of the tract causes loss of sensation below the level of the lesion.

Lateral

Spinothalamic

Tract:

The bilateral section of the tract leads to total loss of pain and temperature sensations on both sides below the lesion.

The unilateral lesion causes loss of pain (analgesia) and temperature (

thermoanesthesia

) below the level of the lesion

o

n the opposite side. The contralateral sensory loss extends to a level one segment below that of the lesion owing to the oblique crossing of fibers.

Slide21

DIFFERENCES BETWEEN DCML & ANTEROLATERAL SYSTEM

DCML

Large, myelinated fibersMechanoreceptors.High velocity: upto 70 meters/ sec.Spatial orientation is highly developed. High degree of localization. Transmits the sensations: Tactile localizationTwo-point discriminationPressure Stereognosis Propriception Vibration

ANTEROLATERAL SYSTEM

Small diameter,

myelinated

as well as

unmyelinated

fibers.

Multiple types of receptors.

Low velocity: 1-15 m/sec

Poor spatial orientation. Low degree of localization.

Transmits the sensations:

Pain

Thermal

Itch

Tickle

Crude touch

Crude pressure

Slide22

Slide23

The spinocerebellar tract

The fibers of this pathway convey proprioceptive impulses to the cerebellum. It has 2 divisions:

Anterior

Spinocerebellar

Tract

Posterior

Spinocerebellar

Tract

Slide24

SPINOCEREBELLAR TRACTS

Anterior Spinocerebellar Tract

Proprioceptive information.Also contains fibers from the motor pathways so that the cerebellum is kept informed about the state of the motor neuron activity. Fibers cross over but then cross back again the cerebellar peduncles. Terminate in the cerebellum.

Posterior Spinocerebellar Tract

Uncrossed.

Carries information mainly from the muscle spindle and the tendon organs of the trunk and lower limb, regarding position and movement of individual limb muscles.

Axons enter the posterior gray column and terminate in the

nucleus

dorsalis

(Clark’s column).

Ascend on the same side to terminate in the cerebellar cortex.

Fast conducting.

Slide25

Slide26

Pain suppression “Analgesia” system of the brain

Slide27

The degree to which a person reacts to pain varies tremendously. This results partly from a capability of the brain itself to suppress input of pain signals to the nervous system by activating a pain control system, called an

analgesia system

.

Thus, the analgesia system can block pain signals at the initial entry point to the spinal

cord.

Slide28

ANALGESIA SYSTEM of the Brain

It consists of three major components: The periaqueductal gray and periventricular areas of the mesencephalon and upper pons surround the aqueduct of Sylvius and portions of the third and fourth ventricles. Neurons from these areas send signals to the raphe magnus nucleus, a thin midline nucleus located in the lower pons and upper medulla, and the nucleus reticularis paragigantocellularis, located laterally in the medulla. From these nuclei, second-order signals are transmitted down the dorsolateral columns in the spinal cord to a pain inhibitory complex located in the dorsal horns of the spinal cord. At this point, the analgesia signals can block the pain before it is relayed to the brain.

Slide29

Gate control Theory of Pain

Transmission in nociceptive pathways can be interrupted by actions within the dorsal horn of the spinal cord at the site of sensory afferent transmission. This gate mechanism is operated by a balance between excitation in large and small peripheral nerve fibers. An excess of impulses in large nerve fibers results in the closure of the gate and non-production of pain; on the other hand, relative excess of impulses in small nerve fibers opens the gate and produces pain sensation. Deep and visceral pain can be decreased by applying irritating substances to the skin overlying deep structures. This is the basis of the use of the Counterirritation for the relief of deep and visceral pain.

Slide30

OPIOIDS

Opioids are commonly used analgesics (chemicals that relieve the pain) that can exert their effects at various places in the CNS, including the spinal cord and dorsal root ganglion.

The different opioids are:

Endorphins:

split products of POMC, made in the Pituitary gland as well as CNS. In the CNS, they decrease perception of pain (analgesic). They are up to 30 times more analgesic than morphine.

Enkephalins

:

are synthesized in the

chromaffin

cells of the adrenal medulla & released with

catecholamines

when sympathetic nervous system is

stimulated,e.g

in stress.

Dynorphin

:

has been detected in the duodenum, posterior pituitary and hypothalamus.

There are interneurons in the superficial region of the dorsal root ganglion where nociceptive afferents terminate. Opioid receptors (OR) are located on the terminals of nociceptive fibers and on dendrites of dorsal root horn neurons .

Activation of OR results in a decrease in release of glutamate and substance P leading to reduced transmission of from nociceptive afferents.

Slide31

REFERRED PAIN

Irritation of a visceral organ frequently produces pain that is felt not at that site but in a somatic structure that may be some distance away. Such pain that is referred to a somatic structure is called Referred Pain.

Slide32

REFERRED PAIN

E.g: Cardiac pain may be referred to the right arm, the abdominal region, or even the back, neck or jaw. When pain is referred, it is usually to a structure that developed from the same embryonic segment or dermatome as the structure in which the pain originates. E.g, the arm and heart have the same segmental origin.CONVERGENCE –PROJECTION THEORY: The basis for referred pain may be convergence of somatic and visceral pain fibers on the same second-order neurons in the dorsal horn that project to the thalamus & then to somatosensory cortex.

Slide33

Slide34

HYPERALGESIA

It is an exaggerated response to a noxious stimulus.

Chemicals released at the site of injury further directly activates receptors on sensory nerve endings leading to inflammatory pain. Nociceptors become more SENSITIVE…..There is also release of substance P and bradykinin, which can further sensitize nociceptive terminals.

ALLODYNIA

It is a sensation of pain in response to a normal, painless stimulus.

E.g. painful sensation from a warm shower when the skin is damaged by sunburn.

Damaged nerve fibers undergo sprouting, so fibers from touch receptors synapse on spinal dorsal horn neurons that normally receive only nociceptive input. This explains why painless stimuli can induce pain after injury. The release of substance P and glutamate leads to excessive stimulation of NMDA receptors on spinal neurons, a term called “wind up” that leads to excessive activity of pain transmitting pathway.

Slide35

Somatosensory cortex

It

is the area of the cerebral cortex that receives primary sensory impulses directly from the relay centers in thalamus. It has 3 parts:

Somatosensory Area –I

Somatosensory Area- II

Association Cortex

The term

somesthetic

cortex is reserved for Somatosensory Area-I only.

Slide36

Slide37

Somatosensory cortex- I

It is also called the Primary

Somesthetic area.It comprises of area 3,1,2.The sequence of distribution of body areas is represented by a sensory homunculus which is a small figure of a man showing the size of the various parts of the body in proportion to distribution. Lips occupy the greatest area followed by the face and the thumb. This is because many more receptors lie in the lips than in any other part of the body.

Somatosensory cortex- II

Its function is not well known.

It seems to be concerned more with the

spinothalamic

tract and pain sensibility.

It further elaborates the sensory input received by Somatosensory Area I.

Somatosensory Association Area:

These are

Brodmann’s

area 5 & 7.

It receives information from area I & II and also from the visual cortex and the auditory cortex and thalamus.

This area is responsible for decoding the sensory information.

Removal of this area causes

amorphosynthesis

(loss of appreciation of form of objects).

Slide38

THE SENSORY HOMUNCULUS

Slide39

What happens when Area-I is damaged?

The sense of fine touch, position,

stereognosis

are most affected. Higher functions are lost. Crude touch is intact which shows that this is done in the thalamus.

Two-point discrimination is decreased.

Subject cannot judge the weight of an object.

Astereognosis

occurs.

Fine grade changes in temperature are not appreciated.

Orientation of different body parts relative to each other is lost. (Proprioception)

Pain is least affected but is poorly localized and poorly graded.

Slide40

PHANTOM LIMB PAIN

It is defined as pain felt by an amputee that seems to be located in the missing limb. The theory explaining it is that brain can recognize if sensory input is cut off. The area of the brain that once received input from the leg and foot now responds to stimulation of the stump, in exactly the same way it did when the limb was attached. Mirror box therapy is used for treatment of Phantom limb pain.