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Transcript
Chapter Eight
Movement
Control of Movement
Muscles and Their Movements
Fast Muscles
fast contractions but easily fatigued
Used for rapid activity
Slow Muscles
slow contractions but resistant to fatigue
Used for walking, nonstrenuous activity
Control of Movement
Muscles and their Movement
Muscle Control by Proprioceptors
proprioceptors-receptor that is sensitive to the position or
movement of a part of the body
muscle spindle-receptor parallel to the muscle that
responds to the stretch of the muscle
golgi tendon organ-responds to increases in muscle
tension
Figure 8.5 Two kinds of proprioceptors regulate the contraction of a muscle
When a muscle is stretched, the nerves from the muscle spindles transmit an
increased frequency of impulses, resulting in a contraction of the surrounding
muscle. Contraction of the muscle stimulates the Golgi tendon organ, which
acts as a brake or shock absorber to prevent a contraction
that is too quick or extreme.
Units of Movement
Voluntary Movements
most movements are a combination of voluntary and
involuntary (ex: walking)
Involuntary Movements
Reflexes-consistent automatic responses to stimuli
Brain Mechanisms of Movement
Cerebral Cortex
Primary Motor Cortex-stimulation along this cortex can elicit
coordinated movements
Posterior Parietal Cortex-some neurons respond to visual or
somatosensory stimuli, some respond mostly to current or
future movements, or some respond to stimulus/response
mixtures
Prefrontal cortex-responds to sensory signals that lead to a
movement
Premotor cortex-most active during preparations for a
movement
Supplementary motor cortex-most active during preparations
for a rapid series of movements
Figure 8.8 Principal areas of the motor cortex in the human brain
Cells in the premotor cortex and supplementary motor cortex are active
during the planning of movements, even if the movements
are never actually executed.
Connections from the Brain to the Spinal Cord
Dorsolateral Tract
set of axons from primary motor cortex and surrounding areas
also arises from red nucleus
controls movement in peripheral areas (ex: toe)
Ventromedial Tract
many axons from the primary motor cortex and supplementary
cortex, midbrain, reticular formation and vestibular nucleus
controls muscles of the neck, shoulders, and trunk
Figure 8.11 The dorsolateral tract
This tract originates from the primary motor cortex, neighboring areas, and the
red nucleus. It crosses from one side of the brain to the opposite side of the
spinal cord and controls precise and discrete movements of the extremities,
such as hands, fingers, and feet.
Figure 8.12 The ventromedial tract
This tract originates from many parts of the cerebral cortex and several
areas of the midbrain and medulla. It produces bilateral control of trunk
muscles for postural adjustments and bilateral movements such as
standing, bending, turning, and walking.
Cerebellum
Functions
habit formation
timing
attention
coordination of movements
Organization
cells are arranged in precise geometrical patterns
Purkinje cells exist in sequential planes
parallel fibers are parallel to one another but perpendicular to
the planes of the Purkinje cells
Figure 8.14 Cellular organization of the cerebellum
Parallel fibers (yellow) activate one Purkinje cell after another. Purkinje cells
(red) inhibit a target cell in one of the nuclei of the cerebellum (not shown,
but toward the bottom of the illustration). The more Purkinje cells that
respond, the longer the target cell is inhibited. In this way the cerebellum
controls the duration of a movement.
Basal Ganglia
Basal Ganglia
Large subcortical structures in the forebrain
Substructures
Caudate nucleus-receive input from thalamus/cortex
putamen-receive input from thalamus/cortex
globus pallidus-sends information to the thalamus and on
to the motor and premotor cortices
Role in movement
Organize action movements
Selection or inhibition of movements
Control of muscle force
Figure 8.15 Location of the basal ganglia
The basal ganglia surround the thalamus and are surrounded by the cerebral cortex.
Parkinson’s Disease
Symptoms-rigidity, muscle tremors, slow movement, difficulty
initiating movement
Brain Changes-Selective loss of cells in substantia nigra and
amygdala/decrease in dopamine
Possible Causes
genetics
exposure to toxins (MPTP)
smoking decreases risks/these data have been questioned
Figure 8.16 Connections from the substantia nigra: (a) normal and
(b) in Parkinson’s disease
Excitatory paths are shown in green; inhibitory are in red. The substantia nigra’s
axons inhibit the putamen. Axon loss increases excitatory communication to the
globus pallidus. The result is increased inhibition from the globus pallidus to the
thalamus and decreased excitation from the thalamus to the cerebral cortex. People
with Parkinson’s disease show decreased initiation of movement, slow and
inaccurate movement, and psychological depression.
Figure 8.17 Probability of developing Parkinson’s disease if you have a
twin who developed the disease before or after age 50
Having a monozygotic (MZ) twin develop Parkinson’s disease before age 50
means that you are very likely to get it too. A dizygotic (DZ) twin who gets it
before age 50 does not pose the same risk. Therefore early-onset Parkinson’s
disease shows a strong genetic component. However, if your twin develops
Parkinson’s disease later (as is more common), your risk is the same regardless
of whether you are a monozygotic or dizygotic twin. Therefore late-onset
Parkinson’s disease has little or no heritability.
Parkinson’s Disease
L-Dopa Treatment
precursor for dopamine
demonstrates individual effectiveness
does not stop progression of the disease
numerous side effects (nausea, restlessness, sleep
problems, low blood pressure, hallucinations, and
delusions)
Therapies Other Than L-Dopa
antioxidants, dopamine receptor stimulants, glutamate
blockers, neurotrophins, drugs that decrease apoptosis,
pallidotomy, cell transplants
Huntington’s
Symptoms
facial twitch, tremors across body, writhing
Cause
genetic-autosomal dominant gene
huntingtin-abnormal protein found inside the cells of
Huntington’s victims