Download including those activated in the presence of a painful stimulus

W5D3H4: Pain and Reflexes
Learning Objectives
1. Describe pain sensory pathways and relevant molecules
involved in nociception.
2. Outline spinal reflex circuits, including those activated
in the presence of a painful stimulus.
3. Describe the clinical use of reflexes as assays of motor
neuron function and relate changes in pain and somatic
detection to diabetic neuropathies.
LO 1. Describe pain sensory pathways and relevant molecules involved in nociception
nocioceptors
Area on the skin that receptor responds to
rapidly adapting
slowly adapting
rapidly adapting
slowly adapting
LO 1. Describe pain sensory pathways and relevant molecules involved in nociception
Anatomy of nociceptors
LO 1. Describe pain sensory pathways and relevant molecules involved in nociception
Conduction latency
Compound action potentials recoded in
response to peripheral nerve stimulation
LO 1. Describe pain sensory pathways and relevant molecules involved in
nociception
LO 1. Overview of pain response to mechanical injury: Release of protease ->
Bradykinin production -> activation of free nerve endings-> action potential propagated to
spinal cord & axonal branches-> nociceptor axons release substance P and CGRP ->
histamine release -> vasodilation and increased pain sensation.
LO2. Outline spinal reflex circuits, including those activated in the presence of a painful
stimulus.
"Striking the tendon below the patella gives
rise to a sudden extension of the leg, known
as the knee-jerk reflex.”
Sir Michael Foster (1877) Textbook of
Physiology
0
1
2
3
4
NINDS Reflex Assessment Scale
Reflex absent
Reflex small, less than normal; includes a trace
response or a response brought out only with
reinforcement
Reflex in lower half of normal range
Reflex in upper half of normal range
Reflex enhanced, more than normal; includes clonus
LO2. Outline spinal reflex circuits, including those activated in the presence of a
painful stimulus.
Characteristics of Spinal reflexes
Involuntary
Short latency (< 40 ms)
Stereotyped responses
Only require peripheral and spinal
neurons
LO2. Outline spinal reflex circuits, including those activated in the presence of a painful
stimulus.
Physiological Mechanisms Underlying Spinal Reflexes
THE PATELLAR TENDON (KNEE JERK) REFLEX
The patellar tendon (knee jerk) reflex illustrates
a monosynaptic stretch reflex and reciprocal
inhibition of the antagonistic muscle.
Stimulus:
Tap to tendon
stretches
muscle.
Receptor: Muscle
spindle stretches
and fires.
Afferent path: Action
potential travels
through
sensory neuron.
Integrating
center:
Sensory neuron
synapses in
spinal
cord.
Efferent path 1:
Somatic motor neuron
onto
Effector 1: Quadriceps
muscle
Efferent path 2: Interneuron
inhibiting somatic motor neuron
Response: Quadriceps
contracts, swinging
lower leg forward.
Effector 2: Hamstring
muscle
Response: Hamstring
stays relaxed, allowing
extension of leg
(reciprocal inhibition).
LO2. Outline spinal reflex circuits, including those activated in the presence of a painful
stimulus.
THE CROSSED EXTENSOR REFLEX
A flexion reflex in one limb causes extension in the opposite limb. The coordination
of reflexes with postural adjustments is essential for maintaining balance.
Gray matter
White matter
Spinal cord
Spinal cord
Ascending
pathways
to brain
Sensory
neuron
Painful stimulus activates
nociceptor.
Primary sensory neuron enters
spinal cord and diverges.
Nociceptor
One collateral activates
ascending pathways for
sensation (pain) and postural
adjustment (shift in center of
gravity).
Alpha
motor
neurons
Painful
stimulus
Extensors inhibited
Flexors contract,
moving foot away
from painful stimulus.
Extensors
contract as
weight shifts
to left leg.
Flexors inhibited
Withdrawal reflex pulls foot
away from painful stimulus.
Crossed extensor reflex
supports body as weight shifts
away from painful stimulus.
LO2. Outline spinal reflex circuits, including those activated in the presence of a painful
stimulus.
Flexion and Crossed-Extensor Reflexes in arms
Pain!!!
LO 3. Describe the clinical use of reflexes as assays of motor neuron function and relate
changes in pain and somatic detection to diabetic neuropathies.
------------------------------------------------------------------------------------------------------The type or intensity of reflexes are graded according to the following criteria:
Grade
Response
0+
No response or absent reflex
1+
Trace or decreased response
2+
Normal response
3+
Exaggerated or brisk response
4+
Sustained response
-----------------------------------------------------------------------------------------------------Damage to spinal motor neurons, defects in synaptic transmission at the NMJ or
muscle atrophy can result in grades of 0 or 1.
Grades of 3 or 4 can be indicative of damage to the spinal cord or brain, which result
in a condition known as ‘spasticity’ and may include clonus.
LO 3. Describe the clinical use of reflexes as assays of motor neuron function: Spasticity
 Spasticity is a condition characterized by hypertonicity (increased muscle tone),
clonus (a series of rapid muscle contractions), exaggerated tendon jerk reflexes,
involuntary muscle spasms, scissoring (involuntary crossing of the legs), and stiff
joints caused by co-contraction of antagonist muscles.
 The degree of spasticity varies from mild muscle stiffness to severe, painful, and
uncontrollable muscle spasms. Spasticity can interfere with rehabilitation in patients
with certain disorders, and often interferes with daily activities.
 Spasticity is usually caused by damage to brain or spinal neurons involved in the
control of movement. It may occur in association with spinal cord injury, multiple
sclerosis, cerebral palsy, anoxia, brain trauma, severe head injury, and diseases such
as adrenoleukodystrophy, amyotrophic lateral sclerosis (ALS), and phenylketonuria.
 Inferences drawn from an animal model suggest that one of the principal
mechanisms of spasticity is an increase in the excitability of motoneurons
consequent to the lesion in the brain or spinal cord. The increased excitability results
in sustained repetitive discharge of motoneurons in response to brief stimuli.
LO 3. Describe the clinical use of reflexes as assays of motor neuron function:
Clasp-Knife Reflex
 The clasp-knife reflex (also called the inverse myotatic reflex) is a pathological
reflex that is only observed following lesions of the central nervous system that
produce spasticity.
 In response to a rapid muscle stretch, a patient with spasticity first exhibits a strong
stretch reflex, followed by a relaxation of the muscle. It is the sudden release of
muscle tension when a contracting muscle is forcibly stretched that gives the reflex
its name: The spastic limb initially resists flexion (because of the stretch reflex) and
then collapses on itself like the blade of a jack- or clasp-knife.
 The reflex is thought to be mediated by group II and group III afferent fibers arising
from free nerve ending receptors located in muscle fascia and aponeuroses.
 The spinal circuits responsible for the clasp-knife reflex are normally suppressed
and only become operational only after lesions to the spinal cord or brain.
Clonus is the result of a reverberating or exaggerated response
Clonus movie: https://www.youtube.com/watch?v=4SrhgjGIZ30
The following is a good way to conceptualize clonus: If a person standing on the tip ends of
the feet suddenly drops his or her body downward and stretches the gastrocnemius muscles,
stretch reflex impulses are transmitted from the muscle spindles.
Normally this helps you to not land on your heels too hard- as you are able, stand up and try
it!
In clonus, these impulses reflexively excite the stretched muscle, which lifts the body up
again. After a fraction of a second, the reflex contraction of the muscle dies out and the body
falls again, thus stretching the spindles a second time.
Again, a dynamic stretch reflex lifts the body, but this too dies out after a fraction of a
second, and the body falls once more to begin a new cycle. In this way, the stretch reflex of
the gastrocnemius muscle continues to oscillate, often for long periods.
Babinski sign
• A reflex in which there is extension upward of the toes and the
abduction of the toes when the sole of the foot is stroked firmly on
the outer side from the heel to the front
• Normal in infants under the age of 2 years but a sign of brain or
spinal cord injury or disease in older persons.
Watch http://www.youtube.com/watch?v=ZQh6zVxtYGc&feature=related