1. COPYRIGHT © ALLYN & BACON 2012 1 Chapter 8 Control of Movement

2. Skeletal Muscle COPYRIGHT © ALLYN & BACON 2012 2 Anatomy Extrafusal Muscle Fiber one of the muscle fibers responsible for the force exerted by contraction of a skeletal muscle Alpha Motor Neuron A neuron whose axon forms synapses with extrafusal muscle fibers of a skeletal muscle: activation contracts the muscle fibers. Intrafusal Muscle Fiber a muscle fiber that functions as a stretch receptor; arranged parallel to the extrafusal muscle fibers, thus detecting changes in muscle length

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4. 4 Myofibril an element of muscle fibers that consists of overlapping strands of actin and myosin; responsible for muscular contractions

5. 5 Monosynaptic Stretch Reflex a reflex in which a muscle contracts in response to its being quickly stretched; involves a sensory neuron and a motor neuron, with one synapse between them

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7. 7 Figure 8.8 shows a motor homunculus based on the observations of Penfield and Rasmussen (1950).

8. Control of Movement by the Brain COPYRIGHT © ALLYN & BACON 2012 8 Cortical Control of Movement: The Descending Pathways Lateral Group the corticospinal tract, the corticobulbar tract, and the rubrospinal tract Ventromedial Group the vestibulospinal tract, the tectospinal tract, the reticulospinal tract, and the ventral corticospinal tract The ventromedial group consists of the vestibulospinal tract, the tectospinal trac t, the reticulospinal tract, and the ventral corticospinal tract. 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.

9. Control of Movement by the Brain 9 Cortical Control of Movement: The Descending Pathways Corticospinal Tract the system of axons that originates in the motor cortex and terminates in the ventral gray matter of the spinal cord Pyramidal Tract the portion of the corticospinal tract on the ventral border of the medulla Lateral Corticospinal Tract the system of axons that originates in the motor cortex and terminates in the contralateral ventral gray matter of the spinal cord; controls movements of the distal limbs Ventral Corticospinal Tract the system of axons that originates in the motor cortex and terminates in the ipsilateral ventral gray matter of the spinal cord; controls movements of the upper legs and trunk

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11. Control of Movement by the Brain 11 Cortical Control of Movement: The Descending Pathways Corticobulbar Tract a bundle of axons from the motor cortex to the fifth, seventh, ninth, tenth, eleventh, and twelfth cranial nerves; controls movements of the face, neck, tongue, and parts of the extraocular eye muscles The third member of the lateral group is the rubrospinal tract. This tract originates in 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 (as we shall see later) from the cerebellum. Rubrospinal Tract the system of axons that travels from the red nucleus to the spinal cord; controls independent limb movements

12. Control of Movement by the Brain 12 Cortical Control of Movement: The Descending Pathways The second set of pathways originating in the brain stem is the ventromedial group. This group includes the vestibulospinal tracts, the tectospinal tracts, and the reticulospinal tracts, as well as the ventral corticospinal tract (already described). Vestibulospinal Tract a bundle of axons that travels from the vestibular nuclei to the gray matter of the spinal cord; controls postural movements in response to information from the vestibular system Tectospinal Tract a bundle of axons that travels from the tectum to the spinal cord; coordinates head and trunk movements with eye movements

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16. Control of Movement by the Brain 16 Imitating and Comprehending Movements: Role of the Mirror Neuron System Investigators found that neurons in an area of the rostral part of the ventral premotor cortex in the monkey brain (area F5) became active when monkeys saw people or other monkeys perform various grasping, holding, or manipulating movements with objects or when they performed these movements themselves. Thus, the neurons responded to either the sight or the execution of particular movements. The investigators named these cells mirror neurons. Mirror Neurons neurons located in the ventral premotor cortex and inferior parietal lobule that respond when the individual makes a particular movement or sees another individual making that movement

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18. Control of Movement by the Brain 18 Deficits of Skilled Movements: The Apraxias 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 in using a familiar tool or utensil (Leiguarda and Marsden, 2000). Apraxia difficulty in carrying out purposeful movements, in the absence of paralysis or muscular weakness

19. Control of Movement by the Brain 19 The Basal Ganglia Caudate Nucleus a telencephalic nucleus; one of the input nuclei of basal ganglia; involved with control of voluntary movement Putamen a telencephalic nucleus; one of the input nuclei of the basal ganglia; involved with control of voluntary movement Globus Pallidus a telencephalic nucleus; the primary output nucleus of the basal ganglia; involved with control of voluntary movement

20. Control of Movement by the Brain 20 The Basal Ganglia Ventral Anterior Nucleus (of Thalamus) a thalamic nucleus that receives projections from the basal ganglia and sends projections to the motor cortex Ventrolateral Nucleus (of Thalamus) a thalamic nucleus that receives projections from the basal ganglia and sends projections to the motor cortex Subthalamic Nucleus a nucleus located ventral to the thalamus; an important part of the subcortical motor system that includes the basal ganglia; a target of deep-brain stimulation for treatment of Parkinson’s disease

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23. Control of Movement by the Brain 23 Parkinson’s Disease Parkinson’s disease also produces a resting tremor—vibratory movements of the arms and hands that diminish somewhat when the individual makes purposeful movements. The tremor is accompanied by rigidity; the joints appear stiff. However, the tremor and rigidity are not the cause of the slow movements. In fact, some patients with Parkinson’s disease show extreme slowness of movements but little or no tremor. As we saw in Chapter 4, the standard treatment for Parkinson’s disease is L-DOPA, the precursor of dopamine. When an increased amount of L-DOPA is present, the remaining nigrostriatal dopaminergic neurons in a patient with Parkinson’s disease will produce and release more dopamine.

24. Control of Movement by the Brain 24 Huntington’s Disease Another basal ganglia disease, Huntington’s disease, is caused by degeneration of the caudate nucleus and putamen, especially of GABAergic and acetylcholinergic neurons. (See Figure 8.24.) Whereas Parkinson’s disease causes a poverty of movements, Huntington’s disease, formerly called Huntington’s chorea, causes uncontrollable ones, especially jerky limb movements. (The term chorea derives from the Greek khoros, meaning “dance.”) The movements of Huntington’s disease look like fragments of purposeful movements, but occur involuntarily. This disease is progressive and eventually causes death. Huntington’s Disease a fatal inherited disorder that causes degeneration of the caudate nucleus and putamen; characterized by uncontrollable jerking movements, writhing movements, and dementia

25. 25 The symptoms of Huntington’s disease usually begin in the patient’s thirties or forties, but can sometimes begin in the early twenties. The first signs of neural degeneration occur in the caudate nucleus and the putamen— specifically, in the medium-sized spiny inhibitory neurons whose axons travel to the external division of the globus pallidus.

26. Control of Movement by the Brain 26 The Cerebellum The cerebellum is an important part of the motor system. It contains about 50 billion neurons, compared to the approximately 22 billion neurons in the cerebral cortex (Robinson, 1995). Its outputs project to every major motor structure of the brain. When it is damaged, people’s movements become jerky, erratic, and uncoordinated.

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