Task 5 - Motor System PDF

Task 5 - Motor System Learning Goals What is the anatomy of a skeletal muscle? How does a skeletal muscle contract? - added by me, I find it useful to have some understanding. What is a reflex and how does it work? What are different types of reflexes? How do we inhibit reflexes? Which brain structu...

Task 5 - Motor System Learning Goals What is the anatomy of a skeletal muscle? How does a skeletal muscle contract? - added by me, I find it useful to have some understanding. What is a reflex and how does it work? What are different types of reflexes? How do we inhibit reflexes? Which brain structures are involved in different types of movements? What is the structure of the motor system? What are the different motor pathways? How do we learn movements? What are mirror neurons? What motor disorders have been discovered? What is the anatomy of a skeletal muscle? How does a skeletal muscle contract? Skeletal muscles are attached to bones at each end and move the bones when they contract. The attachment is achieved via tendons - strong bands of connective tissue. Flexion - moving a limb toward the body, caused by the contraction of a flexor muscle. Extension - moving a limb away from the body, caused by the contraction of extensor muscles. Synergistic muscles - 2 muscles whose contraction produces the same movement (flexion or extension) Antagonistic muscles - 2 muscles that act in opposition (e.g. biceps & triceps). Anatomy of the skeletal muscles Extrafusal muscle fibers - muscle fibers served by axons of alpha motor neurons. An alpha motor neuron, its axon, and associated extrafusal muscle fibers constitute a motor unit. A single axon of an alpha motor neuron serves several extrafusal muscle fibers. In fingers/eyes muscles, the ratio can be 1:10; in leg muscles it can be 1:100 or more. The units with the fewest fibers permit the highest degree of selective motor control. Intrafusal muscle fibers - muscle fibers that are served by 2 axons - one sensory and one motor. The central region of the intrafusal muscle fiber contains afferent sensory endings that are sensitive to stretch applied to the muscle fiber. The efferent axon of the gamma motor neuron causes the intrafusal muscle fiber to contract, but this contraction contributes a small amount of force. In fact, its function is to modify the sensitivity of the fiber's afferent ending to stretch (see further below - gamma motor system). Extrafusal muscle fibers are found outside the muscle spindles, while intrafusal muscle fibers are found within the spindles. Neuromuscular junction - the synapse between the terminal button of an efferent neuron and the membrane of a muscle fiber. The terminal buttons of the neurons synapse on motor endplates, located in grooves along the surface of the muscle fibers. Endplate potential - when an axon fires, ACh is released by the terminal buttons and produces a depolarization of the postsynaptic membrane. An endplate potential is much larger than an EPSP in between-neuron synapses. It always causes the muscle fiber to fire, propagating the potential along its length, producing a contraction/twitch of the muscle fiber. A single impulse of a motor neuron produces a single contraction of a muscle fiber. The twitches of muscle fibers are an all-or-nothing event, but muscular contraction is not. The strength of a muscular contraction is determined by the average rate of firing of the various motor units. Sensory feedback from muscles There are 2 types of afferent sensory neurons in the muscles: In the intrafusal muscle fibers, the afferent sensory neurons detect muscle length. In the Golgi tendon organ, the stretch receptors detect the total amount of stretch exerted by the muscle, through its tendons. They encode the degree of stretch by the rate of firing. Therefore, they respond to how hard a muscle is pulling (muscle tension, not muscle length). In figure (a), where the muscles are passively lengthened (e.g. if the forearm is slowly being lowered by someone who is supporting it), the rate of firing of MS1 (a muscle spindle afferent neuron) increases, while the afferent activity of the Golgi tendon organ (GTO) remains unchanged. In figure (b), the arm is dropped quickly. MS1 still fires and GTO doesn't. However, Body and Behavior Page 1  In figure (b), the arm is dropped quickly. MS1 still fires and GTO doesn't. However, there is activity in the second type of muscle spindle afferent neuron (MS2), which signals rapid changes in muscle length. In figure (c), weight is suddenly dropped into the hand while the forearm was held parallel to the ground. MS1 and MS2 briefly fire, because the arm quickly comes back to the original position. This time, the GTO fires in proportion to the stress on the muscle, as it monitors the strength of contraction. What is a reflex and how does it work? What are different types of reflexes? How do we inhibit reflexes? Although motor behaviors are controlled by the brain, the spinal cord possesses a certain degree of autonomy. Reflex - a rapid motor response through neural connections located within the spinal cord. The monosynaptic stretch reflex A monosynaptic stretch reflex is a reflex, whose neural circuit consists of only 1 synapse along the route from receptor to effector (see figure (a)). 1. The circuit starts at the muscle spindle, where afferent impulses are conducted to terminal buttons in the gray matter of the spinal cord. 2. These terminal buttons synapse on an alpha motor neuron, which innervates the extrafusal muscle fibers of the same muscle. This reflex performs the following function (see figure (b)): 1. If the weight a person is holding is increased, the forearm begins to move downward. 2. This movement lengthens the muscle and increases the firing rate of the muscle spindle afferent neurons (MSA). 3. The terminal buttons of the MSA stimulate the alpha motor neurons, increasing their rate of firing. 4. The strength of the muscular contraction increases, and the arm pulls the weight up. This reflex also plays a part in maintaining an upright posture (see figure (c)): 1. As we stand, we tend to oscillate forward and back and from side to side. When a person begins to lean forward, the large calf muscle (gastrocnemius) is stretched. 2. This stretching elicits compensatory muscular contraction that pushes the toes downward, thus restoring upright posture. Patellar tendon (knee-jerk) reflex - a sudden stretch in the quadriceps muscle after tapping of the patellar tendon (located just below the kneecap). The knee-jerk reflex is an example of a monosynaptic stretch reflex. The gamma motor system Muscle spindles increase their rate of firing when the muscle is lengthened by a very small amount (they have very high sensitivity). This mechanism is adjustable. When the muscle spindles are relax, they are relatively insensitive to stretch. However, when the gamma motor neurons are active, the spindles become shorter and much more sensitive to changes in muscle length. Imagine a single muscle spindle: ○ When its efferent axon is completely silent, the spindle is completely relaxed and extended. ○ As the firing rate of the efferent axon increases, the spindle contracts and gets shorter. ▪ If the rest of the entire muscle also gets shorter at the same time, there will be no stretch on the central region of the sp indle and the afferent axon will not respond. ▪ However, if the muscle spindle contracts faster than the muscle as a whole, there will be a considerable amount of afferent a ctivity. ○ The motor system uses this phenomenon in the following way: if the brain commands to move a limb, the alpha and gamma motor neurons are activated. The alpha motor neurons start the muscle contraction. ▪ If there is little resistance, both the extrafusal & intrafusal muscle fibers will contract in a similar rate, and little act ivity will be seen from the afferent axons of the muscle spindle. ▪ However, if the limb meets with resistance, the intrafusal muscle fibers will shorten more than the extrafusal muscle fibers, and sensory axons will fire, causing the monosynaptic stretch reflex to strengthen the contraction. Polysynaptic reflexes Body and Behavior Page 2 Polysynaptic reflexes Apart from the monosynaptic stretch reflex, all other reflexes are polysynaptic (the neural circuit that facilitates them contains of >1 synapse). There are 2 populations of afferent axons from the Golgi tendon organ, with different sensitivities to stretch. The more sensitive afferent axons tell the brain how hard the muscle is pulling. The less sensitive ones have an additional function. Their terminal buttons synapse on spinal cord interneurons (neurons that reside entirely within the gray matter of the spinal cord and serve to interconnect other spinal neurons). These interneurons synapse on the alpha motor neurons serving the same muscle. The terminal buttons release glycine and produce IPSPs on the motor neurons. The function of this reflex pathway (inhibitory Golgi tendon organ reflex) is to decrease the strength of muscular contraction when there is danger/damage to the tendons or bones to which the muscles are attached. A decerebrate cat (whose brain stem has been transected - cut through) exhibits decerebrate rigidity - its back is arched and its legs are extended stiffly from the body. This rigidity is a product from excitation originating in the caudal reticular formation, which facilitates all stretch reflexes by increasing the activity of the gamma motor system. Rostral to the brain stem transection is an inhibitory region of the reticular formation that normally counterbalances the excitatory one. The transection removes the inhibitory influence, leaving only the excitatory one. Attempting to flex the outstretched leg of a decerebrate cat will be met with increasing resistance that will suddenly melt away, allowing the limb to flex. This is called the clasp-knife reflex and the sudden release is mediated by the activation of the Golgi tendon organ reflex. Other examples of polysynaptic reflexes are limb withdrawal due to harmful stimulation and the startle reflex. Which brain structures are involved in different types of movements? What is the structure of the motor system? What are the different motor pathways? The motor system is hierarchically organized. Commands cascade down from the cortex to the muscles. The main advantage of this hierarchical organization is that the higher levels of the hierarchy are left free to perform more complex functions. The motor system is also functionally segregated: each level of the system is composed of different neural structures, which perform different functions. Motor association cortex The motor association cortex is at the top of the sensorimotor hierarchy. It contains 2 major areas: the posterior parietal association cortex and the dorsolateral prefrontal cortex. Posterior parietal association cortex The posterior parietal association cortex (the portion of parietal neocortex posterior to the primary somatosensory cortex) plays an important role in integrating information about body part locations and the locations of external objects that the body is going to interact with. By integrating this information, it directs behavior by providing spatial information and directing attention. A large part of the PPAC's output goes to the dorsolateral prefrontal association cortex, various areas of the secondary motor cortex (premotor cortex + SMA) and to the frontal eye field (a small area of prefrontal cortex that controls both eye movements and shifts in attention). Dorsolateral prefrontal association cortex The dorsolateral prefrontal association cortex receives projections from the posterior parietal cortex and it sends projections to areas of secondary motor cortex, primary motor cortex and to the frontal eye field. Body and Behavior Page 3 field. Neurons in many cortical motor areas begin to fire before a motor activity, but those in the dorsolateral prefrontal association cortex tend to fire first. This suggests that decisions to initiate voluntary movements may be made in this area of cortex, but these decisions depend on critical interactions with posterior parietal cortex and other areas of frontal cortex. The secondary motor cortex The secondary motor cortex was thought to only include the supplementary motor area (SMA) and premotor cortex. Recent research shows that there are at least a few more other areas. Areas in the secondary motor cortex receive much of their input from association cortex and send much of their output to primary motor cortex. Neurons in an area of secondary motor cortex often become more active just before the initiation of a voluntary movement and continue to be active throughout the movement. The supplementary motor area is involved in learning and performing sequences of movements. Damage to the SMA disrupts the ability to execute well-learned sequences of responses in which the performance of one response serves as the signal that the next response must be made. Pre-supplementary motor area Premotor cortex The pre-supplementary motor area (pre-SMA) is involved in the Nonarbitrary information - information that specifies just what movement perception of control of spontaneous (voluntary, e.g. moving a finger should be done (e.g. visual information of object location specifies where to whenever you want to) movements. target reaching movement). Electrical stimulation of the motor cortex causes movements, but Arbitrary information - information that is not directly related to the movement they are perceived as automatic and involuntary. In contrast, that it signals (e.g. pointing to a particular object when somebody says its name). electrical stimulation of the medial surface of the frontal lobes The associations between arbitrary stimuli and the movements they designate (including SMA & pre-SMA) often provokes the urge to make a are arbitrary and must be learned. movement or the anticipation that a movement is about to occur. Interesting study: activity of pre-SMA begins 2-3 seconds before The premotor cortex is involved in using arbitrary stimuli to indicate what making a conscious decision to perform a spontaneous movement. movement should be made. This suggests that although we feel that we consciously decide Study: people with damage to the premotor cortex could learn to make when to make a response, the decision is actually made by brain movements in response to nonarbitrary spatial cues (pointing to 1 of 6 processes of which we are unaware. We do not become aware of locations in which they had seen a visual stimulus), but not to arbitrary our decision until it has already been made. cues to make particular movements. Lesions in the posterior parietal cortex disrupt awareness of the intention The premotor cortex is also a component of the mirror neuron system, which is to move. This suggests that the posterior parietal cortex may be involved involved in imitating responses of other people and in understanding and in monitoring one's own plans and intentions rather than directly predicting these actions. informing these intentions. Lesions in the prefrontal cortex (PFC) disrupt people's plans for voluntary action: people can react to events but show deficits in initiating behavior => suggests that PFC is an important source of these decisions. There is evidence that the rostral tip of the cerebral hemispheres - the frontopolar cortex - plays a critical role in deciding to make a motor response. The current view is that the prefrontal cortex plays a critical role in motor decision making. The posterior parietal cortex seems to be involved in storing the information about the decision and transmitting it to the SMA, where the process of executing the response begins. Primary motor cortex The primary motor cortex lies on the precentral gyrus. It shows somatotopic organization (i.e. activation of particular parts of it cause movements of particular parts of the body). This layout is referred to as the motor homunculus. A disproportionate amount of cortical area is devoted to movements of fingers and muscles used for speech. The primary motor cortex is organized in terms of particular movements of parts of the body. Each movement may be accomplished by the contraction of several muscles => complex neural circuitry is located between neurons in the primary motor cortex and the motor neurons in Body and Behavior Page 4  between neurons in the primary motor cortex and the motor neurons in the spinal cord, which cause motor units to contract => the somatotopic organization is looser than it was initially thought. The commands for movement initiated in the motor cortex are assisted and modified - most notably, by the basal ganglia and the cerebellum. A 2007 study found that brief stimulation of particular regions of the primary motor cortex in monkeys caused brief movements, but prolonged stimulation caused much more complex movements (e.g. reaching to grasp, hand to mouth, chewing etc.) The map of these categories was consistent from animal to animal. Reticular formation The reticular formation controls the activity of the gamma motor system and hence regulates muscle tonus (the continuous and passive partial contraction of the muscles). It also plays a role in the control of posture and locomotion (especially the mesencephalic locomotor region, located ventral to the inferior colliculus, which controls the activity of reticulospinal tract neurons). Medulla Different locations in the medulla control (semi)automatic responses such as respiration, sneezing, coughing, and vomiting. Cerebellum The cerebellum projects axons to every major motor structure of the brain. When the cerebellum is damaged, people's movements become jerky, erratic and uncoordinated. The lateral zone of the cerebellum is involved in the control of independent limb movements, especially rapid, skilled movements. Such movements are initiated by neurons in the frontal association cortex, which control neurons in the primary motor cortex. However, the initiating cortices do not contain neural circuitry to calculate the complex sequences of muscular contractions that are needed for rapid, skilled movements (which is done by the lateral cerebellum). When the cerebellum receives information that the motor cortex has begun to initiate a movement, it computes the contribution that various muscles will have to make to perform it. The results are sent to the ventrolateral thalamus, which projects to the primary motor cortex, enabling the cerebellum to modify the ongoing movement that was initiated by the frontal cortex. Damage to the lateral cerebellar zone causes weakness and decomposition of movement: performing separate movements of different joints instead of simultaneous smooth movements. Diffuse damage to the cerebellum impairs the ability to accurately control the direction, force, velocity and amplitude of movements and the ability to adapt patterns of motor output to changing conditions. It is also difficult to maintain steady postures, and attempts to do so usually lead to tremor. Basal ganglia The anatomy of the basal ganglia suggests that they also perform a modulatory function. They do not have many descending motor pathways; instead, they form loops via reciprocal connections with cortical areas and the cerebellum. The basal ganglia can monitor somatosensory information and are informed of movements being planned and executed by the motor cortex. The basal ganglia also participate in learning and in classical conditioning. They are also responsible for movement vigor (the control of speed & amplitude of movement based on motivational factors). The symptoms of Parkinson's disease are caused by degeneration of dopamine-secreting cells in the substantia nigra and subsequent disruption of the afferent pathways to the caudate and putamen. Descending motor pathways Neurons in the primary motor cortex control movements by 2 groups of descending tracts: the dorsolateral (or just lateral) group and the ventromedial group, named for their locations in the spinal cord's white matter. The dorsolateral group consists of the corticospinal, corticobulbar and rubrospinal tracts. It is mostly involved in control of independent limb movements (i.e. left and right limbs make different movements or one remains still, opposite of coordinated movements), particularly of the hands and fingers. The corticospinal tract consists of axons of cortical neurons that terminate in the gray matter of the spinal cord. 1. The axons leave the cortex and travel through subcortical white matter to the ventral midbrain, where they enter the cerebral peduncles. 2. They leave the peduncles in the medulla and form the pyramidal tracts (so called because of their shape). 3. At the caudal medulla, most of the fibers decussate and descend through the contralateral spinal cord, forming the lateral corticospinal tract. The rest of the fibers descend through the ipsilateral spinal cord, forming the ventral corticospinal tract (which is part of the ventromedial group due to its location & function). Most axons in the lateral corticospinal tract originate in the regions of the primary motor cortex and SMA that control the distal parts of the limbs (located far from the body): arms, hands, fingers and the lower legs, feet and toes. They form synapses with motor neurons in the gray matter of the spinal cord, in the lateral part of the ventral horn. These motor neurons control muscles of the distal limbs. Body and Behavior Page 5  muscles of the distal limbs. The axons in the ventral corticospinal tract originate in the upper leg and trunk regions of the primary motor cortex. They control motor neurons that move the muscles of the upper legs and trunk. The corticospinal pathway controls hand and finger movements, especially finger movements when reaching/manipulating. The corticobulbar tract projects to the medulla (sometimes called the bulb). This pathway is similar to the corticospinal tract, except that it terminates in the motor nuclei of the cranial nerves that control movements of the face, neck and tongue and parts of the extraocular eye muscles. The rubrospinal tract originates from the red nucleus (nucleus ruber) of the midbrain. The red nucleus receives its most important inputs from the motor cortex via the corticorubral tract and from the cerebellum. Axons of the rubrospinal tract terminate on motor neurons in the spinal cord that control independent movements of the forearms and hands (i.e. movements that are independent of trunk movements). The ventromedial group originates in the brain stem and consists of the vestibulospinal, tectospinal, reticulospinal and ventral corticospinal tracts. These tracts control more automatic movements: gross movements of the muscles of the trunk and coordinated trunk and limb movements involved in posture and locomotion (movement from one place to another). Neurons of all these tracts receive input from portions of the primary motor cortex that control movements of the trunk and proximal muscles (located on the parts of the limbs close to the body). The vestibulospinal tract starts from the vestibular nuclei. It plays a role in the control of posture. The tectospinal tract starts from the superior colliculus. It is involved in coordinating head and trunk movements with eye movements. The reticulospinal tract's cell bodies are located in many nuclei in the brain stem and midbrain reticular formation. These neurons control several automatic functions, such as muscle tonus, respiration, coughing and sneezing. However, they are also involved in behaviors that are under direct cortical control (e.g. walking). The reticular formation receives a considerable amount of input from the premotor cortex and from several subcortical regions, including the amygdala, hypothalamus, and basal ganglia. Reaching and grasping behavior Body and Behavior Page 6 Reaching and grasping behavior Connections between the parietal lobe and the frontal lobe play a critical role in reaching. Parietal reach region - activated when people were about to make a pointing or reaching movement to a particular location => suggests that the parietal cortex determines the location of the target and supplies information about this location to the motor mechanisms in the frontal cortex. The anterior intraparietal sulcus (aIPS) is involved in controlling hand and finger movements involved in grasping the target object. How do we learn movements? What are mirror neurons? Central sensorimotor programs - patterns of activity programmed into all levels but the highest levels of the sensorimotor system. Complex movements are produced by activating the appropriate combinations of these programs. For example, looking at a magazine causes the association cortex to activate a high-level cortical program that activates lower-level brain stem programs for walking, bending over, picking up and thumbing through. These programs in turn will activate spinal programs that control the muscles to complete the objective. Most of the individual responses made under the lower-level programs are performed without direct cortical involvement, and we are often barely aware of them. Studies in humans show that the involvement of the motor association areas and the cerebellum diminishes for well-practiced sequences compared to a newly learned sequence. Motor equivalence - the same basic movement can be carried out in different ways involving different muscles (e.g. signing one's name with a finger or with a toe on a sandy beach). Motor equivalence demonstrates that the sensorimotor system has some plasticity. There exist programs for behaviors which are adapted to the situation. Central sensorimotor programs for some behaviors can be established by practicing the behaviors. However, the programs for many species-typical behaviors are established without explicit practice. Response-chunking hypothesis - practice combines the central sensorimotor programs that control individual responses into programs that control sequences (chunks) of behavior. Mirror neurons - neurons located in the ventral premotor cortex and the rostral part of the inferior parietal lobule (a region of the posterior parietal cortex). The mirror neuron system is activated when performing an action, seeing someone else performing an action and by sounds that indicate the occurrence of a familiar action. The mirror neuron system is activated most strongly when one watches a behavior in which one is already competent. It develops sensitivity to the sight of movements that a person actually performs, not simply actions that the person has seen performed. Once this sensitivity develops, the circuit is activated by watching another person perform those movements. The mirror neuron system helps us to understand the actions of others. An action is understood when its observation causes the motor system of the observer to "resonate" (i.e. the neurons responsible for performing a particular action are activated when we see someone else beginning to perform that action; feedback from the activation of these circuits gives rise to the recognition of the action). What motor disorders have been discovered? Apraxia - a disorder of voluntary movement caused by damage to the frontal or posterior parietal cortex on the left side of the brain. Apraxia refers to the inability to imitate movements or produce them in response to verbal instructions or inability to demonstrate the movements that would be made using a familiar tool or utensil => it is different from paralysis or weakness that occur when precentral gyrus, basal ganglia, brain stem or spinal cord are damaged. Apraxia patients can often perform movements under natural conditions when they are not thinking about what they are doing. Limb apraxia - problems with movements of arms, hands and fingers. It is characterized by movement of the wrong part of the limb, incorrect movement of the correct part, or correct movements but in the incorrect sequence. Constructional apraxia - difficulty in drawing pictures of or assembling objects. It is caused by lesions of the right parietal lobe. It seems to involve Body and Behavior Page 7  Constructional apraxia - difficulty in drawing pictures of or assembling objects. It is caused by lesions of the right parietal lobe. It seems to involve deficits in perceiving and imagining geometrical relations. Oral apraxia - problems with movements of the muscles used in speech. Apraxic agraphia - a particular type of writing deficit. Huntington's disease - a genetic disorder characterized by abrupt, involuntary movements and profound changes in mental functioning. It is caused by damage to the basal ganglia. Contralateral neglect - a disturbance of a patient's ability to respond to stimuli on the side of the body contralateral to the side of a brain lesion. This disturbance is present in the absence of simple sensory/motor deficits. It is associated with large lesions of the right posterior parietal cortex, though damage to other brain regions has also been implicated. Most patients with contralateral neglect often behave as if the left side of their world (relative to their own bodies) does not exist, and they often fail to realize that they have a problem. Object-based contralateral neglect - some patients also tend not to respond to the left sides of objects, regardless of where the objects are in their visual fields, and even when the objects are presented horizontally or upside down. Astereognosia - deficits in stereognosis (the ability to identify objects by touch). Large lesions to the primary motor cortex can produce astereognosia, the ability to move one body part independently of others, and may reduce speed, accuracy and force of movements. Such lesions to do not, however, eliminate voluntary movement (it is thought that this is due to motor pathways that descend directly from secondary and association motor areas). Muscular dystrophy - a disease that leads to degeneration of and functional changes in the muscles. It is caused by a genetic abnormality. It strikes almost exclusively boys, begins at the age of 4-6 years and usually leads to death in early adulthood. Flaccid paralysis - if the spinal cord is injured, reflexes below the level of injury may be lost. It usually results from a considerable length of the spinal cord has been destroyed. Amyotrophic lateral sclerosis (ALS) - a disease in which the motor neurons of the brain stem and spinal cord spontaneously start to die and their target muscles waste away. This is the disease that Stephen Hawking had. Body and Behavior Page 8