Pain physiology
Nociception Dr. Ashok Solanki )
Everybody experience pain
Sign of underlying disease
Protective phenomenan
26-Jan-16 1Dr. Ashok Solanki
Tpes of painy
 Acute pain may be
 1.Somatic
 2.Visceral
 3.Reffered
 Chronic- long lasting
chronic diseases like arthritis.
26-Jan-16 Dr. Ashok Solanki 2
PAIN - NOCICEPTION
 Introduction
 Types of pain
 Pain receptors
 Pain stimulation
 Fast and slow pain
 Has dual feeling
 Path of both types of pain is different.
 Visceral pain is reffered
 Lateral spinothalamic tract
 Through thalamus in V.P.L.
 PAIN INHIBITORY SYSTEM OF BRAIN
 Sign of many underlying disease or damage.
a) Types of pain (somatic- fast/slow,muscular or visceral)
b) Pain pathway
c) Visceral pain & Referred Pain
d) Analgesic or pain control system of bDefinition of pain
e) Physiology of pain (properties & reaction)
f) rain & spinal cord
g) Clinical
a) Definition of pain
Pain sensation is unpleasant but protective sensation
aroused by noxious stimuli that damage or can damage
body tissues.
b) Physiology of pain (properties and reaction)
Purpose or importance- Protective
Stimulus- noxious (chemicals like- Ach, bradykinin,
serotonin, H,K, PGs or mechanical or thermal)
Receptors- free nerve endings (polymodal receptors)
Adaptation- non or slow adopting receptors
Nerve fibers- fast pain is carried by A-delta nerve fibers
while slow pain by ’C’ type.
NT-- glutamic acid (at spinal cord) for fast pain, subs P (at
spinal cord) for slow pain
Pathway- lateral spinothalamic (neo STT for fast pain
paleo STT for slow pain)
Reaction- pain is associated with muscle spasm,
withdrawal reflex (SC, fast pain), arousal (RF),
unpleasant emotions (limbic system, slow pain) and
autonomic changes- nausea, vomiting, pulse and BP
changes (hypothalamus, slow pain)
Localization & Intensity discrimination- poor but better
for fast pain
c) Pathways of Pain
1) From face- by trigeminal nerve (5 cranial nerve)
2) From esophagus, trachea & pharynx- 9 & 10 CN
(parasympathetic nerves)
3) From thoracic & abdominal viscera- sympathetic
nerves
4) From pelvic region- parasympathetic nerves
5) From skin of rest of the body- by free nerve endings
in lateral spinothalamic tract
VBC Of thalamus
thro. post. limb of IC
Primary sensory cortex
dorsal horn of spinal cord, Marginal nucleus
for fast pain & Substantia gelatinosa for slow
pain
neo STT (fast pain) & paleo STT (slow pain)
Origin, course & crossing
1 order neurons
Arise from receptors (free nerve endings) to dorsal horn
Of spinal cord, Marginal nucleus (MN) for fast pain &
Substantia gelatinosa (SG) for slow pain
2 order neurons
arise from MN & SG, cross to opposite side thro. Ante.
commissure & finally ascend in lateral column of SC as
neo STT (fast pain) & paleo STT (slow pain) & relay at VBC
Of thalamus & nearby st.
3 order neurons
arise from VBC of thalamus (mainly fast & few slow pain
fibers) & terminate at primary sensory cortex (area 3,1,2)
Termination
All fast pain fibers & few (20%) slow pain fibers terminate
at PSC while majority of slow pain fibers, subcortically at
diffuse nuclei of thalamus, tectal nucleus & RF.
Center
Is PSC but is perceived at the level of thalamus & RF
Collaterals
To RF (aurosal), limbic system (emotion) & hypothalamus
(autonomic changes)
Ischemic muscle pain (SN)
- During muscle activity Lewis P factor (adenine, K &
lactic acid) pass from muscle to tissue space & clear
by blood
- But if level of Lewis P factor becomes high (ex-
during exercise) pain starts till it is cleared
Clinical-
i) intermittent claudication (leg pain on walking, when
arteries are blocked),
ii) angina pectoris (chest pain on exercise when coronary
arteries are blocked )
Visceral pain (SN)
Causes-
1. Over distension of hollow viscera (commonest),
2. Ischemia.
3. Obstruction
4. Spasm of hollow viscera.
Pathway-
from via type C autonomic nerves to lateral STT.
Properties-
-cause referred and radiating pain (like viscera to
peritoneum).
-more commonly associated with muscle guarding,
-associated with unpleasant emotions and autonomic
changes (nausea, vomiting, low pulse and low BP.)
-localization & intensity discrimination is poor
-Visceras insensitive to pain-
Parenchyma of liver,
brain tissue
and alveoli of lungs are insensitive to pain.
But liver capsule, bronchi, parietal pleura & meninges
are very sensitive to pain.
Referred Pain (SN)
Referred Pain is the pain that is felt away from the
damaged tissue.
Dermatome rule-
visceral pain is often referred to embryonic
corresponding dermatome. The dermatome and the
visceral are innervated by the nerves arising from the
same spinal segment.
Example-
- Cardiac pain is referred to inside of the left arm.
- Pain of Appendix & ovary is referred to umbilicus,
- Diaphragm to rt. shoulder
1)convergence theory of referred pain
sensory nerve carrying pain sensation from the viscera
and the sensory nerves carrying pain sensation the
dermatome converge on to same second order neuron.
2) Facilitation theory of referred pain
sensory nerve carrying pain sensation from the viscera
via branches (collaterals) stimulate sensory nerve
carrying pain sensation from the dermatome. (produce
subliminal fringe effect)
a) Analgesic or pain control system of brain and spinal
cord Or
Mesenchephalic descending pain suppressing pathway
1. Periaqueductal grey area These fibers cause release of
encephalin & stimulates neurons in raphe nucleus
2. The raphe magnus nucleus These fibers cause release
of serotonin & stimulates neurons in spinal cord
3. Local neurons present in dorsal horns of spinal cord.
These fibers cause release of encephalin.
& encephalin causes presynaptic inhibition of pain fibers
entering into dorsal horn of spinal cord.
Stimulants of
Analgesic system
-fibers from limbic
System,hypothalamus
-Stress, psychological
-Collaterals from pain
pathway,
-Brain opiate system
(endorphins and
encephalin)
The raphe magnus nucleus
in pons (serotonin)
Local neurons present in
dorsal horns (encephalin)
Periaqueductal grey area in
midbrain (encephalin)
presynaptic inhibition of
pain fibers in dorsal horn
b) Gait control theory of pain (dorsal horn of SC)
in the dorsal horn A beta, fine touch fibers cause pre-
Synaptic inhibition of pain fibers & closes the date for
pain sensation.
Role of brain in gate control
Terminals of pain fibers at dorsal horn have opiate
receptors, here descending cortical fibers can also inhibit
pain fibers & close the gate by secreting opiates
Clinical
Hyperalgesia- increase sensitivity to pain is known as
hyperalgesia. It may be due to:
1) primary hyperalgesia- increase sensitivity of
receptors
2) secondary hyperalgesia increase sensitivity of
pathway. (thalamic overreacton)
Hypoalgesia- is decrease sensitivity to pain while
Paralgesia is abnormal pain sensation
Acute pain (good pain) & chronic pain (bad pain)
Two components of pain
Fast pain is acute- 0.1 sec
Sharp pain
pricking
acute pain
burning pain
 Only on superficial part
 Short duration
 Highly localized
Slow pain 1 sec later
 Slow burning
 Aching pain
 Throbbing pain
 Chronic pain
 Prolongrd
 Tissue damage or organ
 Poory localized
26-Jan-16 23Dr. Ashok Solanki
Common causes of pain
 Rise in body temp above 45
 Some chemical –bradykinin
 Tissue ischemia- lack of oxygen
 Muscular spasm
 Inflammation
 5 Cardinal signs of inflammation Heat,
swelling, redness, tenderness, loss of function.
 Pain has psychological aspects.
26-Jan-16 24Dr. Ashok Solanki
Nociceptirs- and their stimulation
 Free nerve endings
 Widespread
 Stimuli- mechanical, electrical, chemical.
 Permanent or short duration.
 Slow adaptation nature
 Protective
 Rate of tissue damage
26-Jan-16 25Dr. Ashok Solanki
Pain has dual pathways
1. The sharp fast pain pathway
2. Slow – chronic pain pathway.
3. Fast by small type A delta fiber
4. Slow by type C fibers– 0.5 to 2 m/sec
5. Stimulus gives double sensation
6. Terminates on dorsal horns
7. Carried to the brain
26-Jan-16 Dr. Ashok Solanki 26
THE ANALGESIA SYSTEM
 PREAQUEDUCTAL GRAY
 RAPHE MAGNUS NUCLEUS
 PAIN INHIBITORY COMPLEX IN
DORSAL HORNS
Referred Pain – why away from
the site of origin?
 Dermatomal Rule-
embriological devlopment of
embriyo.
plasticity in the CNS coupled with
convergence of peripheral and visceral
pain fibers on the same second-order
neuron that projects to the brain.
26-Jan-16 Dr. Ashok Solanki 28
26-Jan-16 Dr. Ashok Solanki 29
Dorsal Column–Medial
Lemniscal System
 1. Touch sensations requiring a high degree of
localization of the stimulus
 2. Touch sensations requiring transmission of
fine gradations of intensity
 3. Phasic sensations, such as vibratory
sensations
 4. Sensations that signal movement against the
skin
 5. Position sensations from the joints
 6. Pressure sensations having to do with fine
degrees
 of judgment of pressure intensity
26-Jan-16 Dr. Ashok Solanki 30
Area S1
Anterolateral
Pathway
Anterior
and
Lateral
Division
26-Jan-16 Dr. Ashok Solanki 31
Characteristics of Transmission in the
Anterolateral Pathway
 the velocities of transmission are only one third
 the degree of spatial localization of signals is
poor;
 the gradations of intensities are also
 far less accurate
 the ability to transmit rapidly changing or
 rapidly repetitive signals is poor.
 is a cruder type of transmission system than the
dorsal column–medial lemniscal system.
26-Jan-16 Dr. Ashok Solanki 32
PAIN CONTROL (ANALGESIA)
 THE ANALGESIA SYSTEM
 THE BRAIN’S OPIATE SYSTEM
 INHIBITION OF PAIN BY TACTILE
STIMULATION
 TREATMENT OF PAIN BY ELECTRICAL
STIMULATION
 REFERED PAIN
Dr. Ashok Solanki 34
Distribution of Referred Pain
Dr. Ashok Solanki 36
Tuesday, January 26, 2016 37
26-Jan-16 Dr. Ashok Solanki 38
26-Jan-16 Dr. Ashok Solanki 39
26-Jan-16 Dr. Ashok Solanki 40
Structurally distinct areas, called Brodmann’s areas, of the
human
cerebral cortex.
 DIVISIBLE INTO 50 AREAS.
26-Jan-16 Dr. Ashok Solanki 41
Referred Pain
 Not at the site but superficial part of skin.
 Deep somatic pain may also be referred
 cardiac pain to the inner aspect of the left
arm
 tip of the shoulder caused by irritation of
the central portion of the diaphragm
 Important clinical sign for clinician.
 Follows the Dematological rule.
26-Jan-16 Dr. Ashok Solanki 42
26-Jan-16 Dr. Ashok Solanki 43
26-Jan-16 Dr. Ashok Solanki 44
26-Jan-16 Dr. Ashok Solanki 45
26-Jan-16 Dr. Ashok Solanki 46
26-Jan-16 Dr. Ashok Solanki 47
Three major pathways carry sensory
information
– Posterior column pathway
– Anterolateral pathway
– Spinocerebellar pathway
Role of Formation, Thalamus, Cerebral
Cortex
 cortex plays an especially important role in
interpreting pain quality
 strong arousal effect
 a cordotomy in the thoracic region of the
spinal cord often relieves the pain
 cauterize specific pain areas in the
intralaminar nuclei in the thalamus
26-Jan-16 Dr. Ashok Solanki 49
Transmission of Less Critical
Sensory Signals in the
Anterolateral Pathway
 Carries following sensations
 Pain
heat,
 Cold
 crude tactile
 Tickle
 Itch
 sexual sensations
26-Jan-16 Dr. Ashok Solanki 50
26-Jan-16 Dr. Ashok Solanki 51
PALEOSPINOTHALMIC TRACT
for transmitting slow- chronic pain
 Slow –chronic type C fibers
 Lamina 2 and 3 of dorsal horns
 Joined by lamina 5.
 To anterior commissure
 To the opposite side of the cord
 To the brain through anterolateral pathway
 Substance P – the NT.
26-Jan-16 Dr. Ashok Solanki 52
Pain Suppression
26-Jan-16 Dr. Ashok Solanki 53
Neospinothalamic tract
 Terminate mainly in lamina 1.
 Fast A delta fibers
 Cross immediately opposite side.
 To anterior commissure
 Upwards passing to brain
 Called anterolateral column.
 Glutamate – the NT.
26-Jan-16 Dr. Ashok Solanki 54
26-Jan-16 Dr. Ashok Solanki 55
26-Jan-16 Dr. Ashok Solanki 56
Projection of the Paleospinothalamic
Pathway
 terminates widely in the brain stem
 Only one tenth to one fourth of the fibers pass all the way
to the thalamus
 most terminate in one of three areas
(1) the reticular nuclei of the medulla, pons, and
mesencephalon
(2) the tectal area of the mesencephalon
(3) the periaqueductal gray region surrounding the
aqueduct of Sylvius
Then upward to the thalamus and hypoyhalamus
26-Jan-16 Dr. Ashok Solanki 57
Some Clinical Abnormalities
of Pain
 Hyperalgesia
 Herpes Zoster (Shingles)
 Tic Douloureux
 Brown-Séquard Syndrome
26-Jan-16 Dr. Ashok Solanki 58
26-Jan-16 Dr. Ashok Solanki 59

pain physiology

  • 1.
    Pain physiology Nociception Dr.Ashok Solanki ) Everybody experience pain Sign of underlying disease Protective phenomenan 26-Jan-16 1Dr. Ashok Solanki
  • 2.
    Tpes of painy Acute pain may be  1.Somatic  2.Visceral  3.Reffered  Chronic- long lasting chronic diseases like arthritis. 26-Jan-16 Dr. Ashok Solanki 2
  • 3.
    PAIN - NOCICEPTION Introduction  Types of pain  Pain receptors  Pain stimulation  Fast and slow pain  Has dual feeling  Path of both types of pain is different.  Visceral pain is reffered  Lateral spinothalamic tract  Through thalamus in V.P.L.  PAIN INHIBITORY SYSTEM OF BRAIN  Sign of many underlying disease or damage.
  • 4.
    a) Types ofpain (somatic- fast/slow,muscular or visceral) b) Pain pathway c) Visceral pain & Referred Pain d) Analgesic or pain control system of bDefinition of pain e) Physiology of pain (properties & reaction) f) rain & spinal cord g) Clinical
  • 5.
    a) Definition ofpain Pain sensation is unpleasant but protective sensation aroused by noxious stimuli that damage or can damage body tissues. b) Physiology of pain (properties and reaction) Purpose or importance- Protective Stimulus- noxious (chemicals like- Ach, bradykinin, serotonin, H,K, PGs or mechanical or thermal) Receptors- free nerve endings (polymodal receptors) Adaptation- non or slow adopting receptors Nerve fibers- fast pain is carried by A-delta nerve fibers while slow pain by ’C’ type.
  • 6.
    NT-- glutamic acid(at spinal cord) for fast pain, subs P (at spinal cord) for slow pain Pathway- lateral spinothalamic (neo STT for fast pain paleo STT for slow pain) Reaction- pain is associated with muscle spasm, withdrawal reflex (SC, fast pain), arousal (RF), unpleasant emotions (limbic system, slow pain) and autonomic changes- nausea, vomiting, pulse and BP changes (hypothalamus, slow pain) Localization & Intensity discrimination- poor but better for fast pain
  • 7.
    c) Pathways ofPain 1) From face- by trigeminal nerve (5 cranial nerve) 2) From esophagus, trachea & pharynx- 9 & 10 CN (parasympathetic nerves) 3) From thoracic & abdominal viscera- sympathetic nerves 4) From pelvic region- parasympathetic nerves 5) From skin of rest of the body- by free nerve endings in lateral spinothalamic tract
  • 8.
    VBC Of thalamus thro.post. limb of IC Primary sensory cortex dorsal horn of spinal cord, Marginal nucleus for fast pain & Substantia gelatinosa for slow pain neo STT (fast pain) & paleo STT (slow pain)
  • 9.
    Origin, course &crossing 1 order neurons Arise from receptors (free nerve endings) to dorsal horn Of spinal cord, Marginal nucleus (MN) for fast pain & Substantia gelatinosa (SG) for slow pain 2 order neurons arise from MN & SG, cross to opposite side thro. Ante. commissure & finally ascend in lateral column of SC as neo STT (fast pain) & paleo STT (slow pain) & relay at VBC Of thalamus & nearby st.
  • 10.
    3 order neurons arisefrom VBC of thalamus (mainly fast & few slow pain fibers) & terminate at primary sensory cortex (area 3,1,2) Termination All fast pain fibers & few (20%) slow pain fibers terminate at PSC while majority of slow pain fibers, subcortically at diffuse nuclei of thalamus, tectal nucleus & RF. Center Is PSC but is perceived at the level of thalamus & RF Collaterals To RF (aurosal), limbic system (emotion) & hypothalamus (autonomic changes)
  • 11.
    Ischemic muscle pain(SN) - During muscle activity Lewis P factor (adenine, K & lactic acid) pass from muscle to tissue space & clear by blood - But if level of Lewis P factor becomes high (ex- during exercise) pain starts till it is cleared Clinical- i) intermittent claudication (leg pain on walking, when arteries are blocked), ii) angina pectoris (chest pain on exercise when coronary arteries are blocked )
  • 12.
    Visceral pain (SN) Causes- 1.Over distension of hollow viscera (commonest), 2. Ischemia. 3. Obstruction 4. Spasm of hollow viscera. Pathway- from via type C autonomic nerves to lateral STT. Properties- -cause referred and radiating pain (like viscera to peritoneum). -more commonly associated with muscle guarding,
  • 14.
    -associated with unpleasantemotions and autonomic changes (nausea, vomiting, low pulse and low BP.) -localization & intensity discrimination is poor -Visceras insensitive to pain- Parenchyma of liver, brain tissue and alveoli of lungs are insensitive to pain. But liver capsule, bronchi, parietal pleura & meninges are very sensitive to pain.
  • 15.
    Referred Pain (SN) ReferredPain is the pain that is felt away from the damaged tissue. Dermatome rule- visceral pain is often referred to embryonic corresponding dermatome. The dermatome and the visceral are innervated by the nerves arising from the same spinal segment. Example- - Cardiac pain is referred to inside of the left arm. - Pain of Appendix & ovary is referred to umbilicus, - Diaphragm to rt. shoulder
  • 16.
    1)convergence theory ofreferred pain sensory nerve carrying pain sensation from the viscera and the sensory nerves carrying pain sensation the dermatome converge on to same second order neuron.
  • 17.
    2) Facilitation theoryof referred pain sensory nerve carrying pain sensation from the viscera via branches (collaterals) stimulate sensory nerve carrying pain sensation from the dermatome. (produce subliminal fringe effect)
  • 18.
    a) Analgesic orpain control system of brain and spinal cord Or Mesenchephalic descending pain suppressing pathway 1. Periaqueductal grey area These fibers cause release of encephalin & stimulates neurons in raphe nucleus 2. The raphe magnus nucleus These fibers cause release of serotonin & stimulates neurons in spinal cord 3. Local neurons present in dorsal horns of spinal cord. These fibers cause release of encephalin. & encephalin causes presynaptic inhibition of pain fibers entering into dorsal horn of spinal cord.
  • 20.
    Stimulants of Analgesic system -fibersfrom limbic System,hypothalamus -Stress, psychological -Collaterals from pain pathway, -Brain opiate system (endorphins and encephalin) The raphe magnus nucleus in pons (serotonin) Local neurons present in dorsal horns (encephalin) Periaqueductal grey area in midbrain (encephalin) presynaptic inhibition of pain fibers in dorsal horn
  • 21.
    b) Gait controltheory of pain (dorsal horn of SC) in the dorsal horn A beta, fine touch fibers cause pre- Synaptic inhibition of pain fibers & closes the date for pain sensation. Role of brain in gate control Terminals of pain fibers at dorsal horn have opiate receptors, here descending cortical fibers can also inhibit pain fibers & close the gate by secreting opiates
  • 22.
    Clinical Hyperalgesia- increase sensitivityto pain is known as hyperalgesia. It may be due to: 1) primary hyperalgesia- increase sensitivity of receptors 2) secondary hyperalgesia increase sensitivity of pathway. (thalamic overreacton) Hypoalgesia- is decrease sensitivity to pain while Paralgesia is abnormal pain sensation Acute pain (good pain) & chronic pain (bad pain)
  • 23.
    Two components ofpain Fast pain is acute- 0.1 sec Sharp pain pricking acute pain burning pain  Only on superficial part  Short duration  Highly localized Slow pain 1 sec later  Slow burning  Aching pain  Throbbing pain  Chronic pain  Prolongrd  Tissue damage or organ  Poory localized 26-Jan-16 23Dr. Ashok Solanki
  • 24.
    Common causes ofpain  Rise in body temp above 45  Some chemical –bradykinin  Tissue ischemia- lack of oxygen  Muscular spasm  Inflammation  5 Cardinal signs of inflammation Heat, swelling, redness, tenderness, loss of function.  Pain has psychological aspects. 26-Jan-16 24Dr. Ashok Solanki
  • 25.
    Nociceptirs- and theirstimulation  Free nerve endings  Widespread  Stimuli- mechanical, electrical, chemical.  Permanent or short duration.  Slow adaptation nature  Protective  Rate of tissue damage 26-Jan-16 25Dr. Ashok Solanki
  • 26.
    Pain has dualpathways 1. The sharp fast pain pathway 2. Slow – chronic pain pathway. 3. Fast by small type A delta fiber 4. Slow by type C fibers– 0.5 to 2 m/sec 5. Stimulus gives double sensation 6. Terminates on dorsal horns 7. Carried to the brain 26-Jan-16 Dr. Ashok Solanki 26
  • 27.
    THE ANALGESIA SYSTEM PREAQUEDUCTAL GRAY  RAPHE MAGNUS NUCLEUS  PAIN INHIBITORY COMPLEX IN DORSAL HORNS
  • 28.
    Referred Pain –why away from the site of origin?  Dermatomal Rule- embriological devlopment of embriyo. plasticity in the CNS coupled with convergence of peripheral and visceral pain fibers on the same second-order neuron that projects to the brain. 26-Jan-16 Dr. Ashok Solanki 28
  • 29.
  • 30.
    Dorsal Column–Medial Lemniscal System 1. Touch sensations requiring a high degree of localization of the stimulus  2. Touch sensations requiring transmission of fine gradations of intensity  3. Phasic sensations, such as vibratory sensations  4. Sensations that signal movement against the skin  5. Position sensations from the joints  6. Pressure sensations having to do with fine degrees  of judgment of pressure intensity 26-Jan-16 Dr. Ashok Solanki 30
  • 31.
  • 32.
    Characteristics of Transmissionin the Anterolateral Pathway  the velocities of transmission are only one third  the degree of spatial localization of signals is poor;  the gradations of intensities are also  far less accurate  the ability to transmit rapidly changing or  rapidly repetitive signals is poor.  is a cruder type of transmission system than the dorsal column–medial lemniscal system. 26-Jan-16 Dr. Ashok Solanki 32
  • 33.
    PAIN CONTROL (ANALGESIA) THE ANALGESIA SYSTEM  THE BRAIN’S OPIATE SYSTEM  INHIBITION OF PAIN BY TACTILE STIMULATION  TREATMENT OF PAIN BY ELECTRICAL STIMULATION  REFERED PAIN
  • 34.
  • 35.
  • 36.
  • 37.
  • 38.
  • 39.
  • 40.
  • 41.
    Structurally distinct areas,called Brodmann’s areas, of the human cerebral cortex.  DIVISIBLE INTO 50 AREAS. 26-Jan-16 Dr. Ashok Solanki 41
  • 42.
    Referred Pain  Notat the site but superficial part of skin.  Deep somatic pain may also be referred  cardiac pain to the inner aspect of the left arm  tip of the shoulder caused by irritation of the central portion of the diaphragm  Important clinical sign for clinician.  Follows the Dematological rule. 26-Jan-16 Dr. Ashok Solanki 42
  • 43.
  • 44.
  • 45.
  • 46.
  • 47.
  • 48.
    Three major pathwayscarry sensory information – Posterior column pathway – Anterolateral pathway – Spinocerebellar pathway
  • 49.
    Role of Formation,Thalamus, Cerebral Cortex  cortex plays an especially important role in interpreting pain quality  strong arousal effect  a cordotomy in the thoracic region of the spinal cord often relieves the pain  cauterize specific pain areas in the intralaminar nuclei in the thalamus 26-Jan-16 Dr. Ashok Solanki 49
  • 50.
    Transmission of LessCritical Sensory Signals in the Anterolateral Pathway  Carries following sensations  Pain heat,  Cold  crude tactile  Tickle  Itch  sexual sensations 26-Jan-16 Dr. Ashok Solanki 50
  • 51.
  • 52.
    PALEOSPINOTHALMIC TRACT for transmittingslow- chronic pain  Slow –chronic type C fibers  Lamina 2 and 3 of dorsal horns  Joined by lamina 5.  To anterior commissure  To the opposite side of the cord  To the brain through anterolateral pathway  Substance P – the NT. 26-Jan-16 Dr. Ashok Solanki 52
  • 53.
  • 54.
    Neospinothalamic tract  Terminatemainly in lamina 1.  Fast A delta fibers  Cross immediately opposite side.  To anterior commissure  Upwards passing to brain  Called anterolateral column.  Glutamate – the NT. 26-Jan-16 Dr. Ashok Solanki 54
  • 55.
  • 56.
  • 57.
    Projection of thePaleospinothalamic Pathway  terminates widely in the brain stem  Only one tenth to one fourth of the fibers pass all the way to the thalamus  most terminate in one of three areas (1) the reticular nuclei of the medulla, pons, and mesencephalon (2) the tectal area of the mesencephalon (3) the periaqueductal gray region surrounding the aqueduct of Sylvius Then upward to the thalamus and hypoyhalamus 26-Jan-16 Dr. Ashok Solanki 57
  • 58.
    Some Clinical Abnormalities ofPain  Hyperalgesia  Herpes Zoster (Shingles)  Tic Douloureux  Brown-Séquard Syndrome 26-Jan-16 Dr. Ashok Solanki 58
  • 59.