Transcript chapt10_lecture09

Chapter 10
Vander’s
Human Physiology
The Mechanisms of Body Function
Tenth Edition
by
Widmaier • Raff • Strang
© The McGraw-Hill Companies, Inc.
Figures and tables from the book, with additional comments by:
John J. Lepri, Ph. D.,
The University of North Carolina at Greensboro
Figure 10-1
Motor commands
from the brain have
been modified by
a variety of
excitatory and
inhibitory control
systems, including
essential feedback
from sensory
afferent neurons,
along with vision
and balance cues
(not shown).
Planned
Voluntary
Movement
Association
Cortex
*Voluntary
movements,
learned
skills
Motor
Cortex
Loss of voluntary movement
& spastic paralysis (stroke)
Parkinson’s disease/dystonia
Basal
Ganglia
Proprioception
Reticulospinal
Cerebellum
Vestibulospinal
lateralmedial
medullarypontine
Flexors
Extensors
Extensors
Spinal
Reflexes
Skin,
Muscle,
Joint
*Automatic
movements,
postural
adjustments
Ataxia
Nystagmus
Force  # action potentials/motor unit,
and # motor units active
Stretch
Motor
=
motor neurone + its muscle
Unit
Pain
fibres
*Rapid,
Large, fast, fatigable/
protecti
Small, slow, fatigue-resistant
ve
reflexes
Movement
Flaccid paralysis
Neuropathies
ICBruce2002
Figure 10-2
Side and cross-sectional views of some of the
neural components regulating motor commands.
Altered processing abilities in these components
can cause motor problems such as Parkinsonism.
Figure 10-3
Examples of the
categories of
information and
their
underlying
neuronal
substrates
modifying the
production of
motor commands
from the brain.
One motor unit consists of a
single motor neurone and the
muscle fibres it innervates.
Precisely controlled muscles,
like the extraocular muscles,
have low “Innervation ratios”
(number of muscle fibres per
motor neurone).
Less precisely controlled muscles,
like the postural muscles of the
back, have high innervation
ratios.
Each motor unit is controlled by
descending pathways from the
brainstem & motor cortex.
More action potentials in one motor
unit produce more force (frequency
code). Precise control of force, as in
suturing a wound.
More motor units active at the same
time produce more force (population
code). Gross control of force, as in
carrying a suitcase.
Diseases of the motor unit (such as
motor neurone disease, myasthenia
gravis, or the muscular dystrophies),
produce muscle weakness.
Figure 10-4
Acting on local reflex
circuits and by relaying
impulses to the brain,
muscle spindles and
Golgi tendon organs
provide information
about muscle position
and stretch in order
to finely regulate the
speed and intensity
of muscle contraction.
Regardless of the reason for a change in length, the stretched
spindle in scenario (a) generates a burst of action potentials as
the muscle is lengthened; in scenario (b), the shortened
spindle produces fewer action potentials from the spindle.
13-19: (a) Activation of alpha motor neurons shortens the extrafusal
muscle fibers; if the muscle spindle becomes slack, it no longer signals
muscle length. (b) Activation of gamma motor neurons contracts the
poles of the spindle, keeping its sensitivity.
Figure 10-6
Tapping the patellar tendon
lengthens the stretch
receptor in the associated
extensor muscle in the
thigh; responses include:
compensatory contraction
in that muscle (A and C),
relaxation in the opposing
flexor (B), and sensory
afferent delivery to the brain.
Note: NMJ = neuromuscular junction
Activation of Golgi
tendon organs.
Compared to when a
muscle is contracting,
passive stretch of the
relaxed muscle produces
less stretch of the tendon
and fewer action
potentials from the Golgi
tendon organ.
13-21: Muscle proprioceptors: (a) Spindles are parallel to the
extrafusal fibers, GTOs are in series. (b) GTOs sense increased
tension on the muscle.
Figure 10-8
Contraction of the extensor
muscle on the thigh tenses
the Golgi tendon organ and
activates it to fire action
potentials. Responses
include:
Inhibition of the motor
neurons that innervate this
muscle (A), and excitation
in the opposing flexor’s
motor neurons (B).
Note: NMJ = neuromuscular junction
13-22: Reverse
myotatic reflex.
The neural components of the
pain-withdrawal reflex in this
example proceed as follows:
1 Pain sensory afferents
detect pain in foot and
send action potentials via
dorsal horn of spinal cord.
2 Interneurons in the cord
activate flexor muscles
on the “pained” side of
the body and extensor
muscles on the opposite
side of the body.
3 Muscles move body away
from painful stimulus.
Figure 10-9
Planned
Voluntary
Movement
Association
Cortex
*Voluntary
movements,
learned
skills
Motor
Cortex
Loss of voluntary movement
& spastic paralysis (stroke)
Parkinson’s disease/dystonia
Basal
Ganglia
Proprioception
Cerebellum
*Automatic
movements,
postural
adjustments
Reticulospinal
Vestibulospinal
medullary pontine
lateral medial
Flexors
Ataxia
Nystagmus
Extensors
Extensors
Spinal
Reflexes
Stretch
Pain
Force  # action potentials/motor unit,
and # motor units active
Motor
Unit
= motor neurone + its muscle fibres
Large, fast, fatigable/
Small, slow, fatigue-resistant
Skin,
Muscle,
Joint
Movement
*Rapid,
protective
reflexes
Flaccid paralysis
Neuropathies
ICBruce2002
Figure 10-13
Motor activity must be informed about the body’s
center of gravity in order to make adjustments
in the level of stimulation to muscles whose
contraction prevents unstable conditions (falling).
Extensive neural networks between the major
“motor areas” of the cerebral cortex permit
fine control of movement, utilizing sensory and
intentional signals to activate the appropriate
motor neurons at an appropriate level of stimulation.
Figure 10-10
Efferent motor commands from the cerebral cortex
are contralateral or “crossed,” meaning that the
left cortex controls
the muscles on
the right side of
the body (and
vice versa),
whereas the
brainstem
influences
ipsilateral
(same side)
motor activity.
Figure 10-12
Somatotopic Map
The location and relative size of the cartoon bodyshapes represent the location and relative number
of motor-related neurons in the cerebral cortex.
Planned
Voluntary
Movement
Association
Cortex
*Voluntary
movements,
learned
skills
Motor
Cortex
Loss of voluntary movement
& spastic paralysis (stroke)
Parkinson’s disease/dystonia
Basal
Ganglia
Proprioception
Cerebellum
*Automatic
movements,
postural
adjustments
Reticulospinal
Vestibulospinal
medullary pontine
lateral medial
Flexors
Ataxia
Nystagmus
Extensors
Extensors
Spinal
Reflexes
Stretch
Pain
Force  # action potentials/motor unit,
and # motor units active
Motor
Unit
= motor neurone + its muscle fibres
Large, fast, fatigable/
Small, slow, fatigue-resistant
Skin,
Muscle,
Joint
Movement
*Rapid,
protective
reflexes
Flaccid paralysis
Neuropathies
ICBruce2002
THE VERY END