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

acts as a brake or shock absorber to prevent a contraction 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