chapter eight movement. control of movement muscles and their movements fast muscles fast...
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Chapter EightMovement
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Control of Movement
Muscles and Their MovementsFast Muscles
fast contractions but easily fatiguedUsed for rapid activity
Slow Musclesslow contractions but resistant to fatigueUsed for walking, nonstrenuous activity
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Control of Movement
Muscles and their MovementMuscle 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
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Figure 8.5 Two kinds of proprioceptors regulate the contraction of a muscleWhen 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.
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Units of Movement
Voluntary Movements
most movements are a combination of voluntary and involuntary (ex: walking)
Involuntary Movements
Reflexes-consistent automatic responses to stimuli
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Brain Mechanisms of Movement
Cerebral CortexPrimary Motor Cortex-stimulation along this cortex can elicit
coordinated movementsPosterior 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
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Figure 8.8 Principal areas of the motor cortex in the human brainCells in the premotor cortex and supplementary motor cortex are active
during the planning of movements, even if the movements are never actually executed.
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Connections from the Brain to the Spinal Cord
Dorsolateral Tractset of axons from primary motor cortex and surrounding areasalso arises from red nucleuscontrols movement in peripheral areas (ex: toe)
Ventromedial Tractmany axons from the primary motor cortex and supplementary
cortex, midbrain, reticular formation and vestibular nucleuscontrols muscles of the neck, shoulders, and trunk
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Figure 8.11 The dorsolateral tractThis 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.
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Figure 8.12 The ventromedial tractThis 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.
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Cerebellum
Functionshabit formationtimingattentioncoordination of movements
Organizationcells are arranged in precise geometrical patternsPurkinje cells exist in sequential planesparallel fibers are parallel to one another but perpendicular to
the planes of the Purkinje cells
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Figure 8.14 Cellular organization of the cerebellumParallel 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.
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Basal Ganglia
Basal GangliaLarge subcortical structures in the forebrainSubstructures
Caudate nucleus-receive input from thalamus/cortexputamen-receive input from thalamus/cortexglobus pallidus-sends information to the thalamus and on
to the motor and premotor corticesRole in movement
Organize action movementsSelection or inhibition of movementsControl of muscle force
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Figure 8.15 Location of the basal gangliaThe basal ganglia surround the thalamus and are surrounded by the cerebral cortex.
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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 Causesgeneticsexposure to toxins (MPTP)smoking decreases risks/these data have been questioned
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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.
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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.
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Parkinson’s Disease
L-Dopa Treatmentprecursor for dopaminedemonstrates individual effectivenessdoes not stop progression of the diseasenumerous side effects (nausea, restlessness, sleep
problems, low blood pressure, hallucinations, and delusions)
Therapies Other Than L-Dopaantioxidants, dopamine receptor stimulants, glutamate
blockers, neurotrophins, drugs that decrease apoptosis, pallidotomy, cell transplants
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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