Transcript Neuroanatomy/Pain Review

Neuroanatomy/Pain Review
Anatomy
Dendrite
Cell body (in ganglion)
 nucleus
 Dendrites

Synapse
Body
axon
Anatomy Cont.

Axons (actual nerve fibers)
peripheral nervous system: may be covered
by myelin sheath (schwann cell) which allows
for regrowth
 CNS: oligodendrocytes are the “myelin” but it
doesn't allow for regrowth

Anatomy Cont.

Nodes of Ranier: breaks in myelin. Action
potentials jump from node to node
(salutatory condition) myelin acts as
resistance and insulation and thus needs
nodes for function.
Nerve Types

Afferent; sensory nerves (ascending tracts)
AA Beta): sensory, large diameter with
myelin (Fastest)
 A delta: pain fibers, smaller with less myelin (430m/s)
 C: pain, smallest, non myelinated (.5-2m/s) dull
slow pain
 See Prentice Table 1-2 for Classes of Afferent
Neurons
 Note: First pain is from Adelts (faster), second
pain is C

Nerve Types Cont.

Efferent Nerves: motor nerves
(descending tracts)


Gamma: motor neuron
Ascending and descending tracts:
myelination increases conduction velocity
 Diameter increases conduction velocity (less
resistance)

Nerve Types:

Afferent Nerves
C
Adelta
A Beta
CNS
Physiology

Excitable Tissue: only nerves and muscles
are excitable tissue due to the fact only
they have a resting membrane potential
Physiology Cont.

Resting membrane Potential: a
chemical and electrical balance with a
pump to aid in return to homeostasis.
at rest membrane in -70 mV to -90 mV
 semipermeable membrane which is
impermeable to Sodium at rest

Physiology Cont.

Sodium Potassium pump keeps the potential
by pump in K+ in and Na+ out
 Na+
want in the cell but if it gets in an action
potential is formed
 to +30 mV (a 100 mV difference)
 hormone , chemical, electrical, thermal or
mechanical factors may create action potentials
 As
athletic trainers we try and change this status
and create an action potential
Threshold
The minimum amount of stimulus
necessary to create an action potential
 Polar: refers to negative

depolarize: less negative
 repolarize: becoming negative
 hyperpolarize: more negative

Physiology Cont.

All or none theory: If stimulus meets the
threshold, action potential will always go to
+30mV, even if supra-threshold stimulus is
given
Physiology Cont.

Refractory period: membrane potential
goes below the resting potential of -70mV
and may not be stimulated for a given
period of time. This limits how many
action potentials may be produced
Absolute refractory period: NO stimulus will
create a response no matter how strong
 Relative refractory period: resting potential is
much lower, therefore a higher stimulus is
needed

Pain
How is this class
affecting your pain
receptors?
Pain
The purpose of pain is as a protective
mechanism. Pain is an unpleasant
sensory and emotional experience
associated with actual or potential tissue
damage:
 The types of pain are

Acute
 Chronic
 Referred

Acute Pain
First pain: carried in A-delta fires: larger
diameter fibers contain myelin, reflex to
get off source, goes to cognitive level
(more discrete - very localized)
 Second Pain: carried in C fibers. Smaller
diameter, non myelinated, slower. (less
discrete - more diffuse)

Acute Pain Treatment

Goal

block the pain through:
 inhibition
 blocking
A fibers (Gate Control)
Chronic Pain:

Any pain which lasts for six months or
more (in athletes we may consider chronic
pain to be pain which is continue from
months but is not in proportion to tissue
injury or activity... i.e... chronic tendinitis
may be long lasting but have organic root)
No real purpose (?)
 numerous by-passes. Also goes to limbic
system (emotional control)- learned response

Chronic Pain

Goals in treating
unlearn the Pain
 Acute pain control techniques are usually
ineffective
 Exercise my affect pain by distraction
 Important to have guidance under a physician

Referred Pain (projected pain)

Felt at other site than injured area
Dermatome (skin represented by nerve root)
 Myotome (muscle innovated by nerve root)
 Sclerotome (bones innovated by nerve root)

Pain Transmission
Acute
Acute Pain
Pain
C-Delta A-Beta
Doral Horn
Noxious Stimulus travel Via A-Delta and Cdelta Fibers to Dorsal Horn (spinal Cord)
Limbic System
& Cortex
Descending Control Mech.
Activated here once noxious
stimuli reaches higher centers
of brain. Incoming stimuli can
be inhibited at various levels
and endoginous opiates released
STT (Spinal
thalamic Tract)
Thalamus and Cortex
location and discrimination
Pain Transmitted to
Higher Brain Centers
Retinacular Formation &
Periaquductal Gray (PAG)
Motor, sensory and autonomic Response
Discrimination and Location of
pain occurs during this sequence
Pain theories
Specificity Theory
 Pattern Theory
 Gate Control Theory

Specificity theory: specific
stimulus has a specific receptor
which goes to a location in the
brain The specific location
identifies the pain’s quality. Thus
any noxious stimulus applied to
the surface of the skin results in a
pain sensation. The evaluation of
the type of pain occurs in the
brain.
Pattern Theory: a pattern or
coding of sensory information
is created by different
sensations. This theory is
faulty due to the number of
different types of receptors
proven to exist.
Gate Control Theory (1965)

Melzack and Wall originally described a
neurophsiologic mechanism which
involved the concept of peripheral and
central “gating”. The gate theory utilizes
the specificity theory and the pattern
theory and added the interaction of
peripheral afferents with a modulation
system in the spinal cord gray matter.
Additionally Melzack and Wall believed
there also exists a descending
modulation system.
Gate Control Theory
First Order neurons: the theory focuses
on the first order neurons (primary
afferents): the A-beta (large diameter
sensory neurons) and A-delta and C
neurons (both small diameter sensory
neurons).
 A non-painful stimulus can block the
transmission of a noxious stimulus

A-beta
C delta
non-painful
Brain/Pain centers
noxious stimulus stimulus
Blocking entry of c-delta Fibers
Gate Control Theory Cont.
The second order neuron, the T-cell and
the substantia gelatinosa (Rexed’s
laminae II and II of the dorsal horn of
the spinal gray matter) can exert affects
on the primary afferent
 Works on the premise that the SG
(located in dorsal horn) modulates
afferent nerve impulses and influence
transmission of T cells. This activates a
central controlling mechanism

Gate Control

In Dorsal Horn of Spinal Cord
Brain
. A-Beta
Sensory, Proprioception, Etc
SG
A-Delta, C Fibers
Pain Transmission
T
Inhibitory Synapse
Facilitator Synapse
The second order neuron
When the substantia gelatinosa is active
the “gate” is closed and there is a
decrease in the amount of sensory input to
the T-cell
 If the S.G. is relatively inactive the “gate” is
open
 the balance of activity in the large and
small diameter sensory neurons
determines the position of the “gate”

Gate Control Theory

Large diameter afferents cause an initial
increase in the T-cells followed by a
reduction of activity. The initial increase
is due to direct activation of the secondorder neuron by primary afferents. The
reduction is an indirect result due to
large-diameter afferents also activating
the s.g. cells which causes the gate to
close
Gate Control Theory Cont.

Small diameter afferents increase T-cell
activity by these primary afferents also
activate inhibitory interneurons that reduce
activity in the s.g which open the gate
Gate Control Theory

When the balance of small to large
diameter sensory neuronal input is no
longer maintained and reaches a critical
value the second-order neurons are
activated. This activation is of the
ascending system and leads to the
perception of pain and the subsequent
behavioral responses.
Gate Control Theory
The Descending control system in which
emotion and past experience evoke
descending input, impinging upon the
gating mechanism to block pain sensation
at the spinal level.
 PAIN is an excellent “bible” for those
working clinically with pain control

Pain modulation: Levels Theory
of Pain Control

Spinal Levels of Pain Control
Gate Control Theory
 Central Biasing (hyperstimulation analgesia)
 Endogenous Opiate (Pituitary level)

Level I: Presynaptic inhibition
Gate Control Theory
The concept that when several sensory
stimuli reach the spinal cord at the
same location and time. one of them
becomes dominant.
 As long as the stimulation is causing
firing of the sensory nerve, the gate to
pain should be closed
 If accommodation occurs (electrical
stimulus) the gate is then open and pain
returns

Level 2: Descending inhibition
Central Biasing

A theory of pain
modulation where
higher centers such
as the cerebral
cortex influence the
perception of and
response to pain
Transmission of sensory
input ot higher
brain centers
Central
 Impulses from higher Control
centers act to close
the gate and block
transmission of the
pain message at the
dorsal horn synapse
A-beta fiber
Afferents
Transmission
Cell +
+
Substantia
+gelitinosa -
A-Delta & C
fiber afferents
Level 3: -Endorphin modulation
Endogenous Opiate

Opiate like substance made by the body
 Norepinephrine
 Seratonin

These opiates inhibit the depolarization of
second order nociceptive nerve fibers
(thus no pain)
Found in substantia gelatinosa - activated in
tract
 Causes degeneration of prostaglandin and
dorsal horn inhibition

 The
purpose of knowing all
the pain control theories is
to use modalities to assess
these pain theories and
decrease the
athlete/patient’s pain