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1
Introduction.
Anatomy
Neurohistology.
Pain control.
Chapter 1
Basic local anesthesia.
Dr/Atef fouda
Prof. Oral & Maxillofacial Surgery
Cairo University
Egypt
Atef A. Fouda.
Prof of Oral & Maxillofacial Surgery
Cairo University
3
Introduction.
‫سنه‬ ‫أغسطس‬ ‫من‬ ‫التاسع‬ ‫في‬ ‫ولد‬1819‫في‬
‫بأمريكا‬ ‫شارلتون‬ ‫مدينة‬.‫ويعتب‬ ‫أسنان‬ ‫طبيب‬‫ر‬
‫استخدم‬ ‫من‬ ‫أول‬‫مخدرة‬ ‫كماده‬ ‫اإليثير‬
‫عام‬ ‫وذلك‬1846‫الجراحية‬ ‫العمليات‬ ‫في‬.
William Thomas Green Morton
4
Local
anesthesia
synthesized
from cocaine.
In 1930
In 1970
The use of local anesthesia by
dentists has been a routine part of
practice.
5
Analgesia means block of pain while anesthesia
means block of all sensations which is actually
resulted.
Terminology
6
7
Neurohistology.
Cell body
Axon
Dendrites
8
Neuron
Neuron is a cell with its cell
membrane elongated [Axon]and
ended with tree like branches called
dendrites, its terminal part have
receptors.
receptors
myelinated Nerve axon
Un
Myelin sheath
Node of ranvier
Cell body
Axon
Dendrites
9
Neuron
Or covered with
interrupted myelin
sheath; myelinated
nerve.
The axon of the neuron
may be uncovered
which called
unmyelinated nerve
axon.
myelinated Nerve axon
Ganglion
Neural
bundle
10
Great number of axons travel together
which called neural bundle.
Each axon ends with neural cell.
Aggregation of cells called ganglion.
All neurons
aggregated in bundles
to form part of the
nerve trunk.
11
The main nerve trunk is composed of :
neural bundles,
blood vessels,
And
Connective Tissue
sheath.
[nerve sheath]
Neuron
Neural
bundle
Blood
vessels
Nerve
sheath
12
1-Unipolar
3-Bipolar
4-Multi polar
2-PseudoUnipolar
13
1234
14
Trigeminal nerve
is a mixed nerve
that contain
sensory, Motor,
pain and
autonomic fibers.
Trigeminal nerve
Autonomic neurons :
Myelinated.
Multipolar type.
Trigeminal nerve
Pain neurons :
Unmyelinated.
Unipolar type.
Trigeminal nerve
Motor neurons :
Myelinated.
Multipolar type.
Trigeminal nerve sensory
neurons :
Myelinated.
Pseudounipolar type.
15
Neuron function
A-delta fibers.
Myelinated ,Thick
Pseudounipolar
Temperature,
pressure,
proprioception
C -fibers
Unmyelinated, Thin.
Unipolar
pain
B- fibers
Unmyelinated
Unipolar
Sympathetic
A-alpha fibers
Myelinated
Multipolar
Motor
16
17
18
Pain pathway
19
Trigeminal ganglion
Sensory stimuli travel
from receptors to the
pons without rely.
20
After rely in the
pons crosses the
midline and travels
to the contralateral
side in the
thalamus.[Trigemin
al luminescus].
The fibers then
travel to end in the
sensory cortex of
the brain.
Specificity theory:
Stat that pain is a specific sensation, with its own sensory apparatus
independent of touch and other senses .
The pain apparatus formed from “C “nerve fibers (thin unmyelinated
fibers).
Pain Pathway
21
Moritz Schiff, in 1876, was first to definitively
formulate the specificity theory of pain when, he
demonstrated that touch and pain sensations traveled
to the brain along separate pathways.
Moritz Schiff
First order neuron:
22
Injury site
[pulp of a tooth]
spinal cord
“Substantia
gelatinosa”
Pain Pathway
Second order neuron:
Spinal cord Thalamus.
23
Pain Pathway
Third order neuron:
Thalamus
Somatosensory cortex.
Spino
thalamic
tract
24
Pain Pathway
First order neuron:
“Substantia gelatinosa”
Second order neuron:
Spinal cord Thalamus.
Third order neuron:
Thalamus Somatosensory cortex.
Spino
thalamic
tract
25
Injury site
[pulp of a tooth]
spinal cord
Pain Pathway
26
Pain modulation
Gate control theory:
In the thalamus pain modulated
according to activity of sensory
fibers(A delta myelinated fibers) and
activity of pain fibers(C nerve fibers).
Pain is divided into:
pain perception (feeling of pain) and
pain reaction (the response to pain).
Thalamus
27
Pain reaction:
Pain reaction depends primarily on the
integration between thalamus and
cerebral cortex. Depressed thalamic
action results in greater tolerance to
pain and subsequently less pain is felt.
28
Pain threshold:
Pain threshold is the point along a curve of increasing perception of
a stimulus at which pain begins to be felt. It is an entirely subjective
phenomenon.
The pain reaction threshold is inversely proportional to pain
reaction. A patient who is hypo reactive is considered to have a high
pain threshold, whereas a patient with a low pain reaction threshold
is hyper reactive.
29
Control of pain:
•Removing the cause.(eliminate source of pain).
•Blocking the pathway of pain.(Local anesthesia).
•Raising the pain threshold.(use of analgesics).
•Cortical depression to prevent pain reaction
(general anesthesia).
30
31
Neurophysiology.
Pharmacology of L.A.
Properties of local anesthetic agents.
Chapter 2
32
Neurophysiology.
Human cell
Cell membrane consists of phospholipids.
The lipid bilayer permits passage of fat soluble
substances.
Other substances enter the cell through protein gates
which propagates along the cell membrane.
33
Sodium ions in high concentration outside
the cell.
When gates open a flow of sodium ions
go through gates until equilibrium
between concentration outside and inside
the cell.
In resting state of cell
membrane the sodium
molecules concentrated
outside of the cell
membrane, while
potassium concentrates
inside the cell .
With resultant
Relative negative charges
created inside the cell
membrane while positive
charges detected outside.
-70mv
Resting state
As a result of external stimulant (pain)the membrane
showed depolarization “the charges reversed on the
membrane sides”
Cell membrane in resting state with positive
charge outside and negative charges inside.
Reversal of polarity
Propagation of action potential
Na
Na
Na
Na Na Na
Na Na
Na
Na
Na
Na
Na
Na
Na
Na
Na
Na NaNa
Na
K
INSIDE
OUTSIDE
40mv
Depolarization
Stimulus
Gate open
Na
Na
Na
Na
Na
Na
Na Na
Na
Aden
osine
Ph
Ph
Ph
Outside
Inside
Repolarization
40
To stop the transmission of pain impulses , the
action potential should be prevented from
propagation.
To prevent the action potential, the influx of
sodium ion through the gates should be
prohibited.
The membrane gates closed by the
action of local anesthetic agents.
Pain control
Membrane expansion theory:
This theory postulates that an increased lateral
pressure within the nerve membrane is
produced by local anesthetic agents. The
increased pressure results in constriction of the
gates preventing sodium influx from outside to
inside the neural axon.
Theories of local anesthesia:
Partial expansion of the cell membrane due to
the effect of local anesthetic agent
42
Sodium channel blockers:
The anesthetic agent attached to
special protein found in the gates of
cell membrane preventing sodium
transfer.
Penetration of local anethetic agent into the cell
membrane gate.
Na
Na Na
Na
Part [1] local anesthesia for dental students

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Part [1] local anesthesia for dental students

  • 1. 1 Introduction. Anatomy Neurohistology. Pain control. Chapter 1 Basic local anesthesia. Dr/Atef fouda Prof. Oral & Maxillofacial Surgery Cairo University Egypt
  • 2. Atef A. Fouda. Prof of Oral & Maxillofacial Surgery Cairo University
  • 4. ‫سنه‬ ‫أغسطس‬ ‫من‬ ‫التاسع‬ ‫في‬ ‫ولد‬1819‫في‬ ‫بأمريكا‬ ‫شارلتون‬ ‫مدينة‬.‫ويعتب‬ ‫أسنان‬ ‫طبيب‬‫ر‬ ‫استخدم‬ ‫من‬ ‫أول‬‫مخدرة‬ ‫كماده‬ ‫اإليثير‬ ‫عام‬ ‫وذلك‬1846‫الجراحية‬ ‫العمليات‬ ‫في‬. William Thomas Green Morton 4
  • 5. Local anesthesia synthesized from cocaine. In 1930 In 1970 The use of local anesthesia by dentists has been a routine part of practice. 5
  • 6. Analgesia means block of pain while anesthesia means block of all sensations which is actually resulted. Terminology 6
  • 8. Cell body Axon Dendrites 8 Neuron Neuron is a cell with its cell membrane elongated [Axon]and ended with tree like branches called dendrites, its terminal part have receptors. receptors
  • 9. myelinated Nerve axon Un Myelin sheath Node of ranvier Cell body Axon Dendrites 9 Neuron Or covered with interrupted myelin sheath; myelinated nerve. The axon of the neuron may be uncovered which called unmyelinated nerve axon. myelinated Nerve axon
  • 10. Ganglion Neural bundle 10 Great number of axons travel together which called neural bundle. Each axon ends with neural cell. Aggregation of cells called ganglion.
  • 11. All neurons aggregated in bundles to form part of the nerve trunk. 11
  • 12. The main nerve trunk is composed of : neural bundles, blood vessels, And Connective Tissue sheath. [nerve sheath] Neuron Neural bundle Blood vessels Nerve sheath 12
  • 14. 14 Trigeminal nerve is a mixed nerve that contain sensory, Motor, pain and autonomic fibers.
  • 15. Trigeminal nerve Autonomic neurons : Myelinated. Multipolar type. Trigeminal nerve Pain neurons : Unmyelinated. Unipolar type. Trigeminal nerve Motor neurons : Myelinated. Multipolar type. Trigeminal nerve sensory neurons : Myelinated. Pseudounipolar type. 15
  • 16. Neuron function A-delta fibers. Myelinated ,Thick Pseudounipolar Temperature, pressure, proprioception C -fibers Unmyelinated, Thin. Unipolar pain B- fibers Unmyelinated Unipolar Sympathetic A-alpha fibers Myelinated Multipolar Motor 16
  • 17. 17
  • 19. 19 Trigeminal ganglion Sensory stimuli travel from receptors to the pons without rely.
  • 20. 20 After rely in the pons crosses the midline and travels to the contralateral side in the thalamus.[Trigemin al luminescus]. The fibers then travel to end in the sensory cortex of the brain.
  • 21. Specificity theory: Stat that pain is a specific sensation, with its own sensory apparatus independent of touch and other senses . The pain apparatus formed from “C “nerve fibers (thin unmyelinated fibers). Pain Pathway 21 Moritz Schiff, in 1876, was first to definitively formulate the specificity theory of pain when, he demonstrated that touch and pain sensations traveled to the brain along separate pathways. Moritz Schiff
  • 22. First order neuron: 22 Injury site [pulp of a tooth] spinal cord “Substantia gelatinosa” Pain Pathway
  • 23. Second order neuron: Spinal cord Thalamus. 23 Pain Pathway
  • 24. Third order neuron: Thalamus Somatosensory cortex. Spino thalamic tract 24 Pain Pathway
  • 25. First order neuron: “Substantia gelatinosa” Second order neuron: Spinal cord Thalamus. Third order neuron: Thalamus Somatosensory cortex. Spino thalamic tract 25 Injury site [pulp of a tooth] spinal cord Pain Pathway
  • 26. 26
  • 27. Pain modulation Gate control theory: In the thalamus pain modulated according to activity of sensory fibers(A delta myelinated fibers) and activity of pain fibers(C nerve fibers). Pain is divided into: pain perception (feeling of pain) and pain reaction (the response to pain). Thalamus 27
  • 28. Pain reaction: Pain reaction depends primarily on the integration between thalamus and cerebral cortex. Depressed thalamic action results in greater tolerance to pain and subsequently less pain is felt. 28
  • 29. Pain threshold: Pain threshold is the point along a curve of increasing perception of a stimulus at which pain begins to be felt. It is an entirely subjective phenomenon. The pain reaction threshold is inversely proportional to pain reaction. A patient who is hypo reactive is considered to have a high pain threshold, whereas a patient with a low pain reaction threshold is hyper reactive. 29
  • 30. Control of pain: •Removing the cause.(eliminate source of pain). •Blocking the pathway of pain.(Local anesthesia). •Raising the pain threshold.(use of analgesics). •Cortical depression to prevent pain reaction (general anesthesia). 30
  • 31. 31 Neurophysiology. Pharmacology of L.A. Properties of local anesthetic agents. Chapter 2
  • 33. Human cell Cell membrane consists of phospholipids. The lipid bilayer permits passage of fat soluble substances. Other substances enter the cell through protein gates which propagates along the cell membrane. 33
  • 34. Sodium ions in high concentration outside the cell. When gates open a flow of sodium ions go through gates until equilibrium between concentration outside and inside the cell.
  • 35. In resting state of cell membrane the sodium molecules concentrated outside of the cell membrane, while potassium concentrates inside the cell . With resultant Relative negative charges created inside the cell membrane while positive charges detected outside. -70mv Resting state
  • 36. As a result of external stimulant (pain)the membrane showed depolarization “the charges reversed on the membrane sides” Cell membrane in resting state with positive charge outside and negative charges inside. Reversal of polarity
  • 38. Na Na Na Na Na Na Na Na Na Na Na Na Na Na Na Na Na Na NaNa Na K INSIDE OUTSIDE 40mv Depolarization Stimulus Gate open
  • 40. 40 To stop the transmission of pain impulses , the action potential should be prevented from propagation. To prevent the action potential, the influx of sodium ion through the gates should be prohibited. The membrane gates closed by the action of local anesthetic agents. Pain control
  • 41. Membrane expansion theory: This theory postulates that an increased lateral pressure within the nerve membrane is produced by local anesthetic agents. The increased pressure results in constriction of the gates preventing sodium influx from outside to inside the neural axon. Theories of local anesthesia: Partial expansion of the cell membrane due to the effect of local anesthetic agent
  • 42. 42 Sodium channel blockers: The anesthetic agent attached to special protein found in the gates of cell membrane preventing sodium transfer. Penetration of local anethetic agent into the cell membrane gate. Na Na Na Na