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The Neurological Control of Movement
Mary ET Boyle, Ph.D. Department of Cognitive Science UCSD
Levels of Control of Movement
• A change in the place or position of the Movement bodyyyp or a body part.
• When neurological control of movement is working correctly we can … do anything!
• If not, movement disorders such as myasthenia gravis, movement apraxia, ALS, Parkinson’s disease, and Huntington’s disease.
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Levels of Control of Movement: Simple to Complex
The simplest movements are reflexive reactions withdrawing your hand after touching a hot stove or blinking when something gets in your eye
more complex than reflexes, but less complex than other skills
maintaining posture, sitting, standing, walking, and eye movement
complex movements can be learned
playing the violin, riding a bike, and operating exercise equipment
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Stimulation of Movement
Most basic level of control is the spinal cord (e.g., spinal reflexes, such as the withdrawal reflex, are solely controlled by the spinal cord).
Next level involves brain stem structures in the hindbrain and midbrain (e.g., visual pursuit of a light stimulus).
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Highest level of control involves the cerebral cortex and structures such as the dorsolateral prefrontal cortex, the primary and secondary motor cortex, and the somatosensory cortex.
Basal Ganglia (main components: striatum, pallidum, substantia nigra, and subthalamic nucleus)
Influences movement by smoothing out and refining it (gets rid of extraneous movement and acts to ensure that the selected movement occurs with sufficient, but not excessive, force); also responsible for muscle tone and postural adjustments.
The corpus striatum and Huntington’s disease – leads to substantial enlargement of the lateral ventricles
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Cerebellum
Plays a central role in translat ing uncoordinate d movements into a skilled action; receives feedback from sensory receptors that monitor movement and brain stem structures that initiate movement.
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Three types of muscle tissue in the body:
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extension flexion
Contraction of Contraction of the triceps muscle biceps muscle (extensor) (flexor) movement brings the extended away from the body limb back toward the body
Skeletal muscle Muscle fibers Myofibrils Myofilaments
Myosin Actin (thick filaments) (thin filaments)
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Neural Control of Muscle Contraction
The motor neurons of the peripheral nervous system control the skeletal muscles. The cell bodies of motor neurons are located in the gray matter of the ventral horn of the spinal cord and in different parts of the brain stem.
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Motor Neurons: Transmission of a Neural Impulse
Transmission of a neural impulse from motor neuron to muscle fiber at the neuromuscular junction—similar to the transm iss ion o f neura l impu lses be tween neurons
Motor neuron releases ACh into the synaptic cleft.
ACh binds to receptor proteins on the postsynaptic membrane (the muscle fiber).
EPSPs are then produced; upon sufficient excitation, an action potential is generated.
Neuronal voltage gated calcium channel
Skeletal muscle sodium c hanne l
Potassium channel
ACH
ACH receptor
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As the action potential travels down the muscle fiber, it increases the permeability of the fiber membrane to Ca2+ ions, which causes myosin heads to form cross bridges with actin filaments.
The myosin heads pivot, causing the myosin and actin filaments to slide past one another.
The Motor Unit
A motor neuron and the muscle fibers it controls form a motor unit
Each branch of an axon synapses with a single muscle fiber.
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Patellar Reflex
The reflex in which tappin g the tendon of the knee stretches one of the muscles that extends the leg, and the resulting muscle contraction causes the leg to kick outward.
Muscle spindle—A structure embedded within an extrafusal muscle fiber than enables the CNS to contract a muscle to counteract the stretching of the extrafusal muscle fiber.
Intrafusal muscle fiber— A muscle fiber that extends the length of the muscle spindle that is surrounded by annulospiral endings (sensory receptors in the central part of the muscle fiber).
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Components of the Monosynaptic Stretch Reflex
When the extrafusal muscle fibers are stretched, so are the intrafusal fibers
stimulates the annulospiral endings, causing them to fire more rapidly
This increased neural activity travels along the Ia fibers of the annulospiral endings
entering the dorsal root of the spinal cord and synapsing with alpha motor neurons.
The Ia fibers have an excitatory influence on alpha motor neurons, causing the extrafusal muscle fibers to contract
A Polysynaptic Reflex
Withdrawal reflex— The automatic withdrawal of a limb from a painful stimulus
the brain can influence the execution of polysynaptic reflexes
the spinal cord can also inhibit reflexes to prevent damage to our muscles
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Golgi Tendon Organs
Receptor located among the fibers of tendons that measures the total amount of force exerted by the muscle on the bone to which the tendon is attached
Enables motor system to control extent of muscle contraction.
Strength of muscle contraction reflects the force exerted by the muscle on the bone—the greater the contraction of the muscle fibers, the greater the force on the bone.
With too much force, Golgi tendon organs reduce the contraction of extrafusal muscle fibers, resulting in the muscle exerting less pressure on the tendon and bone.
Renshaw Cells
An inhibitory interneuron excited by an alpha motor neuron that causes it to stoppg firing, preventing excessive muscle contraction.
CbtCombats muscle damage that can result from fatigue, which results from muscles contracting often in a short period of time.
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Gamma Motor Neurons
A neuron that synapses with intrafusal muscle fibers to produce continuous muscle tension.
Continuous activity of gamma motor neurons produces a constant contraction of extrafusal muscle fibers (muscle tone)
This muscle tone is maintained at all times, except during REM sleep.
The gamma motor system also gives us the ability to anticipate certain movements and react quickly.
Brain Control of Voluntary Movement
• Hierarchically organized • Starts at dorsolateral prefrontal cortex. • Decision maker
• Sensory input primarily integrated by the posterior parietal cortex.
• Learning changes the locus of control over the movements. • Subcortical control. More efficient.
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Dorsolateral Prefrontal Cortex
The top executive in the perception-action cycle in nonhuman primates and humans.
cells in this area integrate sensory information across time with motor actions needed to deal with the information
Secondary Motor Cortex
Cortical area consisting of the supplementary motor and the premotor areas.
Supplemental motor area --involved in the planning and sequencing of voluntary movements (internally generated Premotor cortex plans and stimuli) sequences externally guided movements. Receives input mostly from the visual cortex
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Supplemental motor area Part of the secondary motor cortex.
receives input from the posterior parietal cortex and the somatosensory cortex
Because most movements are guided by both intentions and external stimuli, the connections between the supplementary motor area and the premotor cortex coordinate movement planning.
Cortical Control of Movement
Primary motor cortex: initiates voluntary movements
Directly involved in the control of motor neurons.
Stimulation results in movements involving groups of muscles – not individual muscles.
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Mirror Neurons
Neurons in the primate premotor cortex that are activated by performing an action or by watching another monkey or person performing an action. Also seems to exist in humans, in Broca’s area and the primary motor cortex. Humans learn many actions through the observation and imitation of the actions of others and the mirror neuron system provides a possible mechanism through which observation can be translated into action.
Plasticity of the Primary Motor Cortex
The primary motor cortex shows great plasticity in its response to sensory and motor changes. Any body part has multiple and widely distributed representations in the topography of the primary motor cortex.
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Plasticity of the Primary Motor Cortex
Though the exact mechanism for this plasticity is not known, one possibility is long-term potentiation (LTP), a long-lasting increased excitability in a specific neural circuit caused by repetitive stimulation. May represent learning at the cellular level.
Depen dent on NMDA receptor acti vati on and GABAA receptor inhibition; weakened by the drug scopolamine.
Primary Somatosensory Cortex
The sensory receptors in the muscles and joints send information about the external environment to the somatosensory cortex and the posteri or pari etal cortex. It then goes to the dorsolateral prefrontal cortex, the secondary motor cortex, and then the primary motor cortex. The primary motor cortex then becomes aware of the status of the musc les that must be act ivate d an d the location of the body parts that must be moved in order to exert the right amount of force.
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Posterior Parietal Cortex
Posterior parietal cortex—Cortical area that integrates input from the visual, auditory, and skin senses and relays it to the primary motor cortex, which uses the information to guide our movements. Damage to this area results in difficulty responding to visual, auditory, or somatosensory stimuli presented to the contralateral (opposite) side of the body (contralateral neglect).
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Other Movement Disorders
Apraxia—A movement disorder characterized by missing or inappropriate actions not caused by paralysis or any other motor impairment. Constructional apraxia—A disorder characterized by difficulty drawing pictures or assembling objects. Limb apraxia—An impairment in the voluntary use of a limb caused by damage to the left parietal lobe or the corpus callosum. Apraxia of speech—A disorder characterized by difficulty speaking clearly, caused by damage limited to Broca’s area.
Motor Pathways
The primary motor cortex uses information from the posterior parietal cortex, somatosensory cortex, and secondary motor cortex to initiate movement. From the primary motor cortex and other cortical areas, two fiber tracts travel through the midbrain and hin dbra in an d connect w it h t he PNS in ord er to produce movement.
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Tracts Originating in the Motor Cortex
Corticospinal tract—Motor pathway that controls movements of fingers, hands, arms, trunk, legs, feet. Lateral corticospinal tract—The axons of the corticospinal tract that cross over in the medulla to connect to the opposite side of the spinal cord, controlling the movement of the fingers, hands, arms, lower legs, and feet on the opposite side of the bdbody. Ventral corticospinal tract—The noncrossing axons that control the movements of the trunk and upper legs on the same side of the body. Corticobulbar tract—A motor pathway that controls movements of the face and tongue.
Tracts Originating in the Primary MtMotor Cortex
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Tracts Originating in the Subcortex
Ventromedial tract—One of four motor pathways originating in different parts of the subcortex that control movements of the trunk and limbs. Vestibulospinal tract—A ventromedial tract that plays a central role in posture. TlTectospinal tract—A ventromedial tract that controls upper trunk (shoulder) and neck movements and coordinates the visual tracking of stimuli.
Tracts Originating in the Subcortex
Lateral reticulospinal tract—A ventromedial tract that activates the flexor muscles of the legs. Medial reticulospinal tract—A ventromedial tract that activates the extensor muscles of the legs. Rubrospinal tract—A motor pathway that controls movements of the hdhands, lower arms, lower legs, and feet.
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Tracts Originating in the Subcortex
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The Cerebellum
The brain area responsible for developing rapid, coordinated responses or habits. Located behind and beneath the cerebral cortex; outer surface is extremely convoluted; represents 10% of the brain’s mass, but contains more than half of its neurons. Ballistic movement—A habitual, rapid, well-practiced movement that does not depend on sensory feedback; controlled by the cerebellum.
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The Cerebellum
Input to/output from the cerebellum is conveyed by large bundles of axons called peduncles. Integrates information about motor activity, balance and head position, limb position and extent of muscle contraction and determines whether ongoing movements are devi ati ng from thei r int end ed course. If movements begin to deviate, the cerebellum can correct them by sending signals to other structures, such as the deep cerebellar nuclei.
The Cerebellum
Purkinje cells–An output cell from the cerebellar cortex, which has an exclusively inhibitory effect. BktBasket cell—A cerebe llar neuron thtthat has an iihibitnhibitory influence on Purkinje cells.
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Consequences of Cerebellar Damage
Difficulty maintaining a stable posture, making movements such as walking unsteady, slurred speech, and uncoordinated eye movements. Research suggests that the cerebellum plays a significant role in cognitive behaviors in addition to its role in fine- tuning motor movements and in motor learning. Neurons in the cerebellum are sensitive to alcohol; alcohol intoxication can lead to signs of cerebellar malfunction. See Scientific American Spotlight “Probing Cerebellar Function”
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The Basal Ganglia
Basal Ganglia—Group of structures that integrates movement and controls postural adjustments and muscle tone. Consists of three subcortical nuclei: Caudate nucleus (part of neostriatum) Putamen (part of neostriatum) Globus pallidus (paleostriatum) Corpus striatum—Part of the basal ganglia consisting of the caudate nucleus and putamen.
The Basal Ganglia
Integrates movement through interconnections with the primary motor cortex, the cerebellum, substantia nigra, red nucleus, and other motor centers in the brain. Damage to the basal ganglia results in impairments in muscle tone, postural iibilinstability, poorly integrate d movements, and difficulty performing voluntary movements (e.g., standing and walking).
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The Basal Ganglia
Damage to the Motor System: Parkinson’s Disease
Parkinson’s disease—A degenerative neurological disorder characterized by rigidity of the limbs and muscle tremors. Bradykinesia—A movement disorder characterized by slow movement. Festination—A tendency in a movement disorder to speed up a walking pace to running. Other syypmptoms include: difficult y in sp eaking, lack of facial expression, apathy, lack of spontaneous blinking, cognitive deficits (e.g., problems with learning, memory, attention, and judgment).
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Damage to the Motor System: Parkinson’s Disease
First signs of the disease may include a tremor in one hand or some stiffness in the muscles of a leg Over time, tremors and rigidity worsen; movement becomes increasingly impaired. Motor disturbances are caused by the degeneration of the DA-producing cells of the substantia nigra that synapse with the basal ganglia. Damage to this nigrostriatal dopaminergic system leads to the bradykinesia, whereas the rigidity and tremors are believed to result from excessive activity in a neural loop extending from the ventrolateral thalamus to the primary motor cortex.
Damage to the Motor System: Parkinson’s Disease
Suggested causes: Genetic basis Enceph aliti s Arteriosclerosis Carbon monoxide or manganese poisoning Trauma to the head Syphilitic damage to the brain Environmental toxins
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Damage to the Motor System: Parkinson’s Disease
Possible treatments: Levodopa—L-dopa; a drug converted to DA in the brain, increasing levels of DA depleted by the disease. Effective in decreasing rigidity and improving movement, but less effective in reducing tremors. Higggh dosages can result in schizop hrenic-like syypmptoms.
Damage to the Motor System: Parkinson’s Disease
Possible treatments: Thalamotomy—Psychosurgical treatment that relieves tremors and improves rigidity; does not relieve bradykinesia. Pallidotomy—Psychosurgical treatment that reduces tremors, rigidity, and bradykinesia. Deep brain stimulation Transplantation of fetal tissue into the corpus striatum (highly controversial)
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Damage to the Motor System: Huntington’s Disease
Huntington’s disease—An inherited neurological disorder characterized by a slow, progressive deterioration of motor control, cognition, and emotion. Caused by a dominant, defective gene on the short arm of chromosome 4. Symptoms usually begin between the ages of 30 and 50, usually with a decline in physical activity and loss of interest in activities (apathy).
Damage to the Motor System: Huntington’s Disease
Other symptoms include: involuntary movements of whole limbs or parts of a limb, interference of voluntary movements like walking, writing, swallowing, and speaking, and cognitive deficits (e.g., impaired storage and retrieval of information, poor abstract reasoning, and diminished cognitive flexibility). Symptoms worsen over 15 years or so, and death eventually results from a loss of muscle control.
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Damage to the Motor System: Huntington’s Disease
Inability to control voluntary movements is caused by atrophy of the cerebral cortex and basal ganglia. The death of neurons in the basal ganglia decreases GABA and ACh levels, which increases activity in the nigrostriatal dopaminergic pathway. This causes the appearance of the invol untary movements that characterize the disease.
Terms
Opposing action of skeletal muscles can be illustrated in the extensi on and flexi on of a limb. Contracting an extensor muscle produces extension of the limb (movement away from the body). Contracting a flexor muscle causes flexion (brings the extended limb back toward the body). Muscles that work in opposioppositiontion to each other (e.g ., biceps and triceps) are called antagonistic muscles; muscles whose contraction results in the same movement are called synergistic muscles.
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Muscle fibers—One of the units comprising a skeletal muscle; about 10 to 100 micrometers in diameter. Myofibrils—One of the units comprising a muscle fiber; cylindrical structures about 1 to 2 micrometers across. Myofilament—A component of a myofibril.
There are two kinds of myofilament in myofibrils: Myosin—The protein component of thick myofilaments. Actin—The protein component of thin myofilaments. Sarcomere—The functional unit of a myofibril, consisting of overlapping bands of thick myosin filaments and thin actin filaments. This gives skeletal muscles a striped appearance, which is why they are sometimes called striated muscles.
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Alpha motor neurons—Motor neurons with a long axon that leaves the ventral root of the spinal cord or bibrain stem and synapse wiihth iidiidlndividual muscle fibers. Their axons conduct information rapidly (220 m/second). Extrafusal muscle fiber—A muscle fiber controlled by an alpha motor neuron. Neuromuscular junction—A specialized synapse between an alpha motor neuron and an extrafusal muscle fiber. Motor end plate—The flattened area of an extrafusal muscle fiber where a motor neuron and the muscle fiber synapse.
The Motor Unit
Each branch of an axon synapses with a single muscle fiber. Collectively, a motor neuron and the muscle fibers it controls form a motor unit (an alpha motor neuron and the muscle fibers it controls). When the axon of an alpha motor neuron has few branches and controls only a few muscle fibers, fine motor control is possible. When the axon has many branches and controls many muscle fibers, gross limb movement is possible.
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Muscle Adaptation
Different types of muscles facilitate diverse abilities: Slow-twitch muscle—A muscle fiber that contracts and fatigues slowly; produces slower contractions that can be maintained for long periods of time without fatiguing. Fast-twitch muscle—A muscle fiber that contracts and fatigues quickly; produces rapid contractions that tire quickly. ItInterme ditdiate-tithtwitch muscle—A muscle fiber ththtat contract s at a lower rate than fast-twitch and a higher rate than slow-twitch muscles; produces contractions of moderate speed and duration. We use primarily slow or intermediate-twitch muscles when we stand or walk; fast-twitch muscles when we run.
Reflex Control of Movement
Reflex—A simple, automatic response to a sensory stimulus. Patellar reflex—A reflex in which tapping the tendon of the knee stretches one of the muscles that extends the leg, and the resulting muscle contraction causes the leg to kic k outwar d. Most reflexes are produced by the spinal cord without involvement of the brain.
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Monosynaptic Stretch Reflex
Monosynaptic stretch reflex—A spinal reflex with a single synapse between the sensory receptor and the muscle effector. Muscle spindle—A structure embedded within an extrafusal muscle fiber than enables the CNS to contract a muscle to counteract the stretching of the extrafusal muscle fiber. Intrafusal muscle fiber—A muscle fiber that extends the length of the muscle spindle that is surrounded by annulospiral endings (sensory receptors in the central part of the muscle fiber).
Monosynaptic Stretch Reflex
When the extrafusal muscle fibers are stretched, so are the intrafusal fibers; stimulates the annulospiral endings, causing them to fire more rapidly. This increased neural activity travels along the Ia fibers (or axons) of the annulospiral endings, entering the dorsal root of the spi nal cord and synapsi ng wi th alph a motor neurons. The Ia fibers have an excitatory influence on alpha motor neurons, causing the extrafusal muscle fibers to contract.
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Primary Motor Cortex: Organization
Organization of the Primary Motor Cortex The movement of different body parts is elicited by stimulation of different regions of the primary motor cortex. There is greater cortical representation of some body parts than of others. Body parts that produce precise movements (e. g., hands and mouth) have greater representation than do parts that produce gross movements (e.g., arms and legs).
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