PAIN PATHWAY AND

GATE CONTROL
THEORY OF PAIN
DR.PAPASANI ANIL KUMAR REDDY
FIRST YEAR RESIDENT NEUROSURGERY
DEFINATION OF PAIN

IASP defines pain as

an unpleasant sensory and emotional experience associated with actual or
potential tissue damage, or described in terms of such damage.
When the pain circuits are correctly working they aware us from external or
internal stimuli that would potentially hurt the tissues.
The sensation we perceive should be unpleasant enough, so it cannot be ignored,
and the sensation should continue as long as the stimulus is present.
• Pain and nociception are different phenomena. Pain cannot be
inferred solely from activity in sensory neurons.
 PAIN RECEPTORS AND FIBERS

Aδ fibers are thinly myelinated, so they can conduct a fast pain signal, at 5–
30 m/s.
Aδ nociceptive fibers convey nociceptive information as well as information
coming from intense mechanical or thermal stimulation. This fast pain has
been reported as the first pain, the initial sharp painful sensation just after the
contact with the noxious stimuli.
PAIN RECEPTORS AND FIBERS

• C fibers are related with a slow pain, since these unmyelinated fibers
conduct impulses at less than 2 m/s, normally evoked by thermal,
mechanical, and chemical stimuli.
• This slow pain is also called second pain, and evokes a more diffuse and
longer lasting painful sensation than the pain evoked by the Aδ fibers.
PAIN RECEPTORS AND FIBERS

• In contrast to other sensory receptors of the body, pain receptors adapt very little and
sometimes not at all.
• Under some conditions, excitation of pain fibres become progressively greater, especially
for slow, aching nauseous, pain as the pain stimulation continues, this increase in
sensitivity of the pain receptors is called HYPERALGESIA (PRIMARY).
• Failure of pain receptors to adapt allows the pain to keep the person appraised of a tissue
damaging stimulus as long as it persists.
 CLASSIFICATION
FAST PAIN SLOW PAIN

A.K.A. sharp pain, pricking pain, acute pain, and electric slow burning
Pain pain, aching pain, throbbing pain, nauseous pain,
and chronic pain

Felt on skin and some deeper tissues like periosteum, the Skin and all deeper tissues .
arterial walls, the joint surfaces, and the Associated with tissue destruction
falx and tentorium in the cranial vault.

Fast pain is elicited by the mechanical Multiple types

and thermal types of stimuli of stimuli mechanical, thermal, and chemical (most important)
pain stimuli

Transmitted in the transmitted to the spinal cord by type C fibers at velocities

peripheral nerves to the spinal cord by small type Aδ between 0.5 and 2 m/sec.
fibers at velocities between 6 and 30 m/sec.
DOUBLE PAIN

• Sudden painful stimulus often gives a ‘double pain sensation’.

1) fast sharp pain transmitted by A delta fiber pathway- makes a person react immediately
to remove himself from the stimulus.
2) slow pain by C fiber pathway- becomes greater over time, eventually producing
intolerable pain and making the person keep trying to relieve the cause of pain
TISSUE INJURY

• Injured cells release ATP, Glutamate that activate free nerve endings
• Releases pro-nociceptive substances , substance-P, CGRP, neuropeptide-Y.
• Mast cells recruited that release inflammatory mediators like prostaglandins, bradykinin,
cytokines, serotonin, histamine,
• C fibers
• Chemical stimulus most important for slow pain in tissue destruction.

• chemicals that excite the chemical type of pain are bradykinin (most
painful chemical), serotonin, histamine, potassium ions, acids,
acetylcholine, and proteolytic enzymes.

• prostaglandins and substance P enhance the sensitivity of pain nerve

endings (free nerve endings and non adaptive nerve endings) but do
not directly excite them
• The intensity of pain is also closely correlated with the rate of tissue damage.

• The greater the rate of metabolism of the tissue, the more rapidly the pain appears.

• the intensity of the pain felt correlates with the local increase in potassium ion
concentration or proteolytic enzymes making the nerve membranes more
permeable to ions (DIRECT ATTACK ON NERVE ENDINGS)
DUAL PAIN PATHWAYS IN THE CORD AND
BRAIN STEM—

THE NEOSPINOTHALAMIC TRACT

&
THE PALEOSPINOTHALAMIC TRACT
 THE NEOSPINOTHALAMIC TRACT FOR FAST PAIN

• A DELTA FIBERS
• LAMINA MARGINALIS (1) IN DORSAL HORNS
• SECOND ORDER NEURONS EXCITED
• long fibers that cross immediately to the opposite side of the cord
through the anterior commissure.
• Turn upward, passing to the brain in the anterolateral columns.
 THE NEOSPINOTHALAMIC TRACT TERMINATION

• Few fibers terminate in the retic

THE NEOSPINOTHALAMIC TRACT
• NEOSPINOTHALAMIC TRACT

• BRAINSTEM (few) AND VENTROBASAL COMPLEX OF THALAMUS (most) AND

POSTERIOR NUCLEI

• SOMATOSENSORY CORTEX.
THE NEOSPINOTHALAMIC TRACT

• Terminate in ventrobasal complex along with the dorsal column–medial

lemniscal tract for tactile sensations.

• Simultaneous stimulation of Tactile sensation increase the localization accuracy

of pain.

• Glutamate is the neurotransmitter substance secreted in the spinal cord at the

type Aδ pain nerve fiber endings.
THE PALEOSPINOTHALAMIC TRACT
THE PALEOSPINOTHALAMIC TRACT
 THE PALEOSPINOTHALAMIC TRACT
• the peripheral slow-chronic type C pain fibers

• terminate in the spinal cord almost entirely in laminae II and III of the dorsal horns
(substantia gelatinosa)

• Joins short fiber neurons within the dorsal horns before entering lamina V

• Form long axons that join the fibers from the fast pain pathway, passing first through the
anterior commissure to the opposite side of the cord

• upward to the brain in the anterolateral pathway.

THE PALEOSPINOTHALAMIC TRACT
 THE PALEOSPINOTHALAMIC TRACT
• substance P is neurotransmitter concerned with slow-chronic pain.

• slow-chronic paleospinothalamic pathway terminates widely in the brain stem

• (1)the reticular nuclei of the medulla,pons, and mesencephalon;

(2) the tectal area of the mesencephalon deep to the superior and inferior colliculi;
(3) the periaqueductal gray region surrounding the aqueduct of Sylvius.
 THE PALEOSPINOTHALAMIC TRACT
• Brain stem (3 above mentioned lower centre regions)

• Ventrolateral Thalamic nuclei and hypothalamus.

• Poor capability of precise pain location due to multisynaptic nature.

• In a cordotomy, the pain-conducting tracts of the spinal cord on the side opposite to
the pain are cut in its anterolateral quadrant to interrupt the anterolateral sensory
pathway (done to relieve severe pain eg: in cancer)
ANALGESIC
PATHWAY
ANALGESIC PATHWAY

• (1) The
periaqueductal gray and periventricular areas of the
mesencephalon

• (2) the raphe magnus nucleus, a thin midline nucleus located in the
lower pons and upper medulla
the nucleus reticularis paragigantocellularis,located laterally in the
medulla.

a pain inhibitory complex located in the dorsal horns of the spinal cord
ANALGESIC PATHWAY

Enkephalin and serotonin, are involved in the analgesia system.

They cause both presynaptic and postsynaptic inhibition of type C and type
Aδ pain fibers.

opiate-like natural substances are

β-endorphin,
met-enkephalin,
leu-enkephalin,
dynorphin.
OTHER THEORIES OF PAIN INHIBITION

• Inhibition of Pain Transmission by Simultaneous Tactile Sensory

Signals.

• large-type Aβ sensory fibers from peripheral tactile receptors

LOCAL INHIBITION

• Treatment of Pain by Electrical Stimulation Electrodes in dorsal

sensory columns, periventricular or periaqueductal area of the
diencephalon.
GATE CONTROL THEORY OF PAIN
• Described by MELZACK AND WALL in 1965

• Describes that there is neural gate is seen in spinal cord which opens and closes thereby
regulating sensation of pain perception.

• Adds that psychological factors play a role in pain perception.

• Dorsal horn of spinal cord is regarded as gate.

• A DELTA and C fibers are small diameter neurons which are outsmarted by ABETA
fibers which carry temperature,touch and pressure sensations by closing the gate.
GATE CONTROL THEORY OF PAIN

• A DELTA and C fibers are small diameter neurons which are outsmarted by
ABETA fibers which carry temperature,touch and pressure sensations by closing
the gate.

• Factors that close gate are amount of activity in pain fibers

amount of activity in other peripheral fibers
 messages that descend from brain
GATE CONTROL THEORY OF PAIN
GATE CLOSED BY
GATE OPENED BY
 REFFERED PAIN
• pain in one of the visceral organs often is referred to an area on the body
surface.

• branches of visceral pain fibers are shown to synapse in the spinal cord
on the same second-order neurons that receive pain signals from the
skin.
REFFERED PAIN
VISCERAL PAIN

• highly localized types of damage to the viscera seldom cause severe pain (eg: surgical cut).

• diffuse stimulation of pain nerve endings throughout a viscus causes pain that can be severe (eg:
ischemia, spasm, overdistension).

• Pain insensitive structures ( alveoli, liver parenchyma, brain parenchyma excluding meninges,
vessels ,tentorium)

• Visceral pain pathways to CNS : true visceral pathway and the parietal pathway.
 VISCERAL PAIN

• True visceral pain is transmitted via pain sensory fibers in the autonomic nerve bundles, and
the sensations are referred to surface areas of the body that are often far from the painful organ

• parietal sensations are conducted directly into local spinal nerves from the parietal peritoneum,
pleura, or pericardium, and these sensations are usually localized directly over the painful area.
 VISCERAL PAIN
TRUE VISCERAL PAIN PATHWAY

localizes it in
the dermatomal segment from which
the visceral organ
originated in the embryo,
VISCERAL PAIN
PARIETAL SENSATION PATHWAY

Appendicitis pain in RIF due parietal

Peritoneal irritation and pain in umbilical
Region due to dermatomal distribution.
HYPERALGESIA

• (1) excessive sensitivity of the pain receptors, called primary

hyperalgesia;

• (2) facilitation of sensory transmission, called secondary

hyperalgesia

• Secondary hyperalgesia frequently results from lesions in the spinal

cord or the thalamus.
HYPERALGESIA

SECONDARY HYPERALGESIA

Dejerine–Roussy syndrome or thalamic pain syndrome is a condition

developed after a thalamic stroke, a stroke causing damage to the
thalamus

Transverse myelitis and spinal cord injury may trigger pain pathways
and cause hyperalgesia.
TIC DOULOUREUX (OR TRIGEMINAL NEURALGIA
OR GLOSSOPHARYNGEAL NEURALGIA

• A lancinating or stabbing type of pain occasionally occurs over one side of the face in the sensory
distribution area.

• Lesion may be in brainstem nucleus or peripheral nerve.

• The pain can be blocked by surgically cutting the peripheral nerve from the hypersensitive area.

• Nerve to be dissected just at cranium entry where sensory and motor fibers are far from each other.
BROWN SEQUARD SYNDROME
BROWN SEQUARD SYNDROME
 HEADACHE

• The brain tissues themselves are almost totally insensitive to pain.

• Instead causes paresthesia in representing body parts.

• tugging on the venous sinuses around the brain, damaging the tentorium, or
stretching the dura at the base of the brain can cause intense pain

• type stretching stimulus to the blood vessels of the meninges can cause headache.
( eg, middle meningeal artery to be locally anesthetized during surgery)
 HEADACHE

• Stimulation of pain receptors in the cerebral vault above the tentorium, initiates
pain impulses in the cerebral portion of the fifth nerve

• Pain infront of head

• pain impulses from beneath the tentorium enter the central nervous system
mainly through the glossopharyngeal,vagal, and second cervical nerves

• Occipital headache
 HEADACHE

• Types of intracranial headache:

1. Headache of Meningitis
2. Headache Caused by Low Cerebrospinal Fluid Pressure.
3. Migraine Headache
4. Alcoholic Headache.
 HEADACHE

• Types of extracranial headache:

1. Headache Resulting from Muscle Spasm.

2. Headache Caused by Irritation of Nasal and Accessory Nasal Structures.
3. Headache Caused by Eye Disorders