Chapter 08: Movement
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Chapter 08: Movement

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The control of movement by the body and the brain and a look at diseases of movement.

The control of movement by the body and the brain and a look at diseases of movement.

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Chapter 08: Movement Presentation Transcript

  • 1. Brain Mechanisms of Movement
  • 2. Role of the Cerebral Cortex
    • Primary Motor Cortex
    • Precentral gyrus of the frontal cortex stimulation elicits movements
    • Axons from Primary Motor Cortex go to basal ganglia while other motor axons go to the brainstem & spinal cord
    • Cerebral Cortex & Complex Actions
    • Stimulation of motor cortex elicits complex movement patterns
    • The motor cortex is stimulated when movement is imagined
  • 3. Areas Near the Primary Motor Cortex Posterior Parietal Cortex Primary Somatosensory Cortex Prefrontal Cortex Premotor Cortex Supplementary Motor Cortex
  • 4. Connections from the Brain & Spinal Cord
    • Dorsolateral Tract
    • Axons from the primary motor cortex & red nucleus synapse in the spinal cord
    • Pyramids in medulla contain dorsolateral tract crossing that contralaterally controls movements of the fingers, toes, hands, etc.
  • 5. Connections from the Brain & Spinal Cord
    • Ventromedial Tract
    • Contains axons from the primary motor cortex, supplementary motor cortex, midbrain tectum, reticular formation & the vestibular nucleus
    • Axons from the ventromedial tract go to both sides of the spinal cord & are largely responsible for neck, shoulder, & trunk movements
  • 6. The Role of the Cerebellum
    • Involved in Motor Control & Learned Motor Behavior
    • Linked to Habit Formation, Aspects of Attention, Timing, & Other Psychological Motor Functions
  • 7. The Cerebellum
    • Cellular Organization
    • Receives input from the spinal cord, from each sensory system via the cranial nerve nuclei, & cerebral cortex where it eventually reaches the cerebellar cortex
    • Neurons in the cerebellar cortex are:
    • 1. Arranged in precise geometrical patterns with multiple repetitions of the same unit
    • 2. Action potentials of parallel fibers excite one Purkinje cell after another
    • 3. Purkinje cells inhibit cells of the nuclei of the cerebellum & the vestibular nuclei in the brain stem
    • 4. Output of Purkinje cells control the timing of movements including turning on & off
  • 8. Basal Ganglia
    • Includes: Caudate Nucleus, Putamen, & Globus Pallidus
    • Caudate nucleus & Putamen are input, globus pallidus is output
    • Important for Habit Learning & the Selection of Movement
    • Obsessive-compulsive disorder is linked to increased activity in the caudate nucleus & prefrontal cortex
  • 9. Parkinson’s Disease
    • Symptoms
    • Rigidity, resting tremor, slow movements & difficulty initiating physical & mental activity, cognitive defects in memory & reasoning
    • 1 in 100 with onset after age 50
    • Immediate cause: gradual progressive death of neurons in Substantia Nigra
    • Possible causes: Genetics; MPTP, a chemical that the body converts into MPP (a toxin destroys dopamine neurons; probably a mixture of causes
  • 10. Parkinson’s Disease
    • Standard Treatment
    • L-Dopa
    • Precursor to dopamine
    • Effectiveness varies
    • Doesn’t prevent the loss of dopamine containing neurons & may contribute to the death of neurons
    • Produces harmful side-effects
    • Alternative Treatments
    • Antioxidant drugs
    • Direct dopamine agonists
    • Glutamate antagonists
    • Neurotrophins
    • Apoptosis blockers
    • High frequency electrical stimulation of the Globus Pallidus
    • Surgical damage to the Globus Pallidus or parts of the Thalamus
  • 11. Huntington’s Disease
    • Severe Degenerative Neurological Disorder
    • Symptoms: twitches, tremors, & writing movements; depression, memory deficits, anxiety, hallucinations, delusions, poor judgment, alcoholism, drug abuse, & sexual disorders
    • Affects 1 in 1000
    • Gradual, extensive brain damage especially in the Caudate Nucleus, Putamen, & Globus Pallidus
  • 12. Huntington’s Disease
    • Onset
    • Most often appears between 30 & 50 years
    • The earlier the onset, the faster the deterioration
    • Heredity
    • Caused by an autosomal dominant gene on chromosome 4
    • Abnormal form of huntingtin , a protein found in neurons that interferes with several metabolic pathways