Anaesthesia & Exodontia Third Year

1. Fundamentals of Impulse
Generation and Transmission
Hesham Marei
BDS, MSC, PhD, FDS RCS (Eng)
Oral and Maxillofacial Surgery Dept.
College of Dentistry, Dammam University, KSA.

2. Anatomy and Physiology of the
Nerve cell
 25 billions neurons exist in the HB
 Nerve cell has -70 to -90 mV potential
difference (polarised) because of the
imbalance of ions in-out.

3. Peripheral Nerve Fibers
Involved in Pain Perception
 A-delta fibers – “large”, myelinated
fibers that transmit sharp pain
 C-fibers – small unmyelinated nerve
fibers that transmit dull or aching
pain.

4. Types of nerve fibres
Sequence
of neural
block
Type
Conduction
velocity
(m/sec.)
Function
Diameter
(um)
LA onset?
Bounded
1
C
0.5-2
Pain reflexes
(dull quality)
0.1-1
NO
2
A Delta
12-30
Temperature &
pain reflexes
1-4
Yes
3
B
3-10
Vegetative
nervous system
1-3
No
4
A Beta
30-70
Pressure &
touch reflexes
5-10
Yes
5
A
Alpha
70-120
Motor
reflexes
10-20
Yes

5. The sensory pathway from jaws and teeth
 Sensation from jaws and teeth are conducted through
the sensory fibers of mandibular and maxillary
nerves.
 These fibers receive impulses from their somatic
sensory area and conduct them to their mother cells in
the GG.
 The nerve cells of in the GG receive the stimuli from
the dendrites and convey them through the axon of
the cells which constitute the sensory root of the T.N.

6.  The axons enter the pons where some of them
ends at the principle sensory nucleus and some
descend through the lateral side of the pons to
end near another collection of nerve cells in the
medulla and called accessory sensory nucleus.
 The principle sensory nucleus in the pons
responsible for touch sensations, while the
accessory sensory nucleus in the medulla and
cervical cord is responsible pain and temperature
sensation .

7. Theories of pain sensation
Four main theories have been put forward to
explain how nerve impulses give rise to
the sensation of pain:
 Speciality theory (von Ferry)
 Central summation (pattern) theory
 Sensory interaction theory
 Gate control theory

8. 1.
Speciality theory (von Ferry):


Specific nerve fibres carry information related to
specific sensations (pain, touch, warmth,…)
according to the sensory spots scattered on the
skin.
It fails to explain the neuralgic, phantom, and
referred pain.

9. 2. Central summation (pattern) theory


Goldscheider proposed that pain is not a separate
entity, but results from over-stimulation of other
primary sensations (touch, light, sound, …). Pain
results when the total output of the nerve cell exceeds
a critical level
It failed to recognize the receptor specialization to
different stimuli

10. 3. Sensory interaction theory:


Noordenbos proposed that the rapidly conducting
large fibre pathways inhibit or suppress activity in
slow-conducting small fibre pathways that convey
pain.
It can explain the mechanism of particular types of
pain e.g.: post-herpetic pain and neuralgic pain
(destruction of the major NF)

11. 4. Gate-control theory:
 Melzack and Wall,
1965 proposed that
the gate-control
system of the Tri.
Nerve is located in
the caudal part of the
spinal nucleus, where
the A delta and C
fibres are inhibited by
two pathways:
The activity of the
ascending very fast AB
afferent fibres.
 The descending efferent
impulses originating from
higher centres (thought,
memory, fear or even pain
originating form other
parts).


13. Three Factors Involved in
Opening and Closing the Gate
 The amount of activity in the pain
fibers.
 The amount of activity in other
peripheral fibers
 Messages that descend from the
brain.

14. Conditions That Close the Gate
 Physical conditions
 Medications
 Counter stimulation (e.g., heat, message)
 Emotional conditions
 Positive emotions
 Relaxation, Rest
 Mental conditions
 Intense concentration or distraction
 Involvement and interest in life activities

15. Conditions that Open the Gate
 Physical conditions
 Extent of injury
 Inappropriate activity level
 Emotional conditions
 Anxiety or worry
 Tension
 Depression
 Mental Conditions
 Focusing on pain

16. Physiology of the peripheral nerve
 The function of a nerve is to carry messages from one part
of the body to another. These messages, in the form of
electrical action potentials, are called Impulses.
 Action Potentials are transient depolarization of the
membrane that result from a brief increase in the
permeability of the membrane to sodium, and usually also
from a delayed increase in the permeability to potassium.

17.  Once an impulse is initiated by a stimulus in
any particular nerve fiber, the amplitude and the
shape remain constant, regardless of changes in
the quality of the stimulus or its strength.

18. Electrochemistry of the nerve conduction and impulse propagation

The sequence of events depends on two factors
(1) The concentrations of electrolytes in the axoplasm
(intracellular fluid) and the extracellular fluids.
(2) The permeability of the nerve membrane to sodium
and potassium ions.

19.  At rest, The inside of the nerve membrane
is negatively charged compared to the
positive outside.
In its resting state, the nerve membrane is
Slightly permeable to sodium ions (Sodium
migrates inwardly because both the
concentration (greater outside) and the
electrostatic gradient (+ ions attracted by –
intracellular potential) Only the fact that
the resting nerve membrane is relatively
impermeable to sodium prevents a massive
influx of this ion.

20.  Freely permeable to Potassium ions (k+). k+ remains within the cell
(exoplasm), despite its ability to diffuse freely through the nerve
membrane and concentration gradient, because the negative charge
of the nerve membrane restrains the positively charged ions by
electrostatic attraction.
 Freely permeable to chloride ions (Cl-). Cl- remains outside the nerve
because the electrostatic gradient from inside to outside forces
outward migration.

21.  When membrane potential decreases,
the permeability of the membrane to
sodium increases and sodium ions
passively start to enter the nerve.
This entry of sodium ions creates less
negativity on the interior of the nerve
membrane and thus generate a new
action potential in this manner the
impulse is propagated.

22. Pain stimulus and mechanisms of LA
 Subsequent to
stimulus, membrane
permeability
increases, Na+ gets
in and K+ gets out,
causing
depolarisation and
the potential
becomes +30 to +40
mV (was – 70 mV)

23.  A decrease in negative membrane potential from -70 to
-55 is necessary to reach the firing threshold.
 When the firing threshold is reached, membrane
permeability to sodium increases dramatically and
sodium ions rapidly enters the exoplasm leading to a
reversed in the electrical potential of the nerve to reach
+40mv.

25. Repolarization
 The action potential is terminated when the
membrane repolarizes. This is caused by the
inactivation of the increased permeability to
sodium.
 The movement of sodium ions into the cell
during depolarization and the subsequent
movement of potassium ions out of the cell
during repolarization are passive.

26.  After return of the membrane potential to its
original level (-70mv), a slight excess exists
within the nerve cell, with slight excess of
potassium extracellulary.
 A period of metabolic activity then begins in
which active transfer of sodium ions out of the
cell occurs via the “ Sodium Pump” (0.7msc)

27. Absolute refractory Period
 Depolarisation is followed by refractory period
where no new impulses are accepted.
(the nerve is unable to respond to any other
stimulus, regardless of its strength)

28. Relative Refractory Period
The absolute refractory period is followed by a
period of relative refractory period during
which a new impulse can be initiated but by a
stronger stimulus.

29. Impulse Propagation & Spread
 Unmyelinated Nerve: Slow forward creeping
process
 Myelinated Nerve: Saltatory conduction

30. References




John G. Meechan, Nigel D. Robb, and Robin A.
Seymour. Pain and anxiety control for the conscious
dental patient. Oxford Publisher, 1998.
Malamed, Handbook of Local Anaesthesia. Mosby, c.v.
co. ltd, 5th Edition, 2002.
Paul D. Robinson.1st Edit. 2000,Tooth extraction a
practical guide
Peterson L, Ellis E, Hupp, J and Tucker, M.
Contemporary Oral And Maxillofacial Surgery Mosby,
C.V. Co. Ltd, 4th Edition 2003.