N165: Quiz 3; Unit 3b

  1. Posterior parietal cortex (PPC)
    • Located posterior to sensorimotor cortex, it integrates sensory and motor portions of the brain, processes position of body and objects in space, and controls eye movements.
    • Lesions: Problems with visual-spatial coordination, problems with attention, neglect syndromes
  2. Premotor cortex (PMA)
    • Located just anterior to M1 and inferior to SMA, it controls postural/trunk and large limb muscles, the planning of actions based on sensory cues, and refinement of movements based on sensory input with cerebellum.
    • Lesions: disruption of learned responses to visual cues
  3. Supplementary motor area (SMA)
    • Located just anterior to M1 and superior to PMA, it is involved in planning learned sequences of movements, activity just prior to movement, and has strong connections with subcortical structures.
    • Unilateral lesions: disruption of learned sequences of movement
    • Bilateral lesions: blocks all movement
    • Stimulation: creates strong urge to move
  4. Primary motor cortex (M1)
    • A strip of cortex just anterior to the central sulcus in the frontal lobes, where the primary control of motor movements occurs.
    • M1 contains a body-based motor map similar to the somatotopic representation in S1.
    • M1 controls the execution of movement.
    • Lesions: spastic paralysis
    • Stimulation: executes a movement
  5. Corticospinal (C.S.) tract
    the fibers that connect motor cortex through the spinal cord to motor neurons throughout the body
  6. Lateral corticospinal tract
    • 80% of the C.S. axons cross to other side
    • these generally go to the limbs
  7. Anterior corticospinal tract
    20% of the C.S. axons don’t cross; these generally go to the trunk
  8. Upper motor neurons
    • originate in the M1 motor region of the cerebral cortex and carry motor information down to a specific spinal cord level.
    • The cell bodies of the upper motor neurons are in M1, and their axons make up the corticospinal tract.
    • When upper motor neurons are damaged (either cell bodies in M1 or axons along spinal cord), ‘function goes up’, because at rest the cortex sends inhibitory signals to the lower motor neurons.
    • When a movement is made, the upper motor neurons stop this inhibitory signal to allow the lower motor neurons to fire and produce a movement.
    • With damage to the upper motor neurons, the baseline inhibitory inputs from the cortex is lost, and the lower motor neurons are hyper-active, causing spastic muscles.
  9. Lower motor neurons
    • bring the nerve impulses from the upper motor neurons out to the muscles.
    • The cell bodies are in the spinal cord and send axons to innervate sets of muscle fibers.
    • When lower motor neurons are damaged, ‘function goes down.’ When the lower motor neurons don’t work, there is no way to send a signal to the muscles to tell them to contract.
    • The muscles are flaccid (loose and floppy), and eventually atrophy (waste away) due to loss of neurotrophic (feeding) factors that the lower motor neurons also deliver to the muscle fibers.
  10. Somatotopic organization
    organization that follows a map of the body (i.e., neighboring body parts have neighboring representations in cortex)
  11. Hemiplegia
    total paralysis of the arm, leg, and trunk on the same side of the body, usually from lesions to M1
  12. Hemiparesis
    weakness on one side of the body
  13. Anosognosia
    • a disorder where the patient is unaware of and denies their disability, often associated with paralysis and right dorsal parietal damage (also seen in Anton’s syndrome, eating disorders).
    • Patients typically use confabulations to ‘explain’ why they have the symptoms.
  14. Confabulation
    • basically: lying unintentionally. More technically: a disturbance of memory, defined as the production of fabricated, distorted, or misinterpreted memories about oneself or the world, without the conscious intention to deceive.
    • Certain types of damage to the parietal lobes can cause neglect syndromes that are associated with confabulation.
    • The patient has anosognosia – thus is not aware that he/she has a deficit (e.g., paralysis) – and instead comes up with random/untrue reasons for why he/she doesn’t have an issue (like ‘I just don’t feel like moving’ instead of ‘I am paralyzed).
  15. Anton’s syndrome
    blindness and anosognosia from dorsal occipital damage
  16. Hemispatial neglect
    a syndrome where patients are unaware of the world/themselves/objects/visual scene/etc. on one side of space, usually the left side from damage to right posterior parietal cortex
  17. Gerstmann's syndrome
    a syndrome where patients have finger agnosia (can’t identify what their fingers/toes are), problems with left/right differentiation, and problems with calculation and writing, It is usually caused by damage to inferior part of dominant parietal cortex or can be developmental
  18. Apraxia
    • a disorder of motor planning involving the loss of the ability to carry out learned purposeful movements, despite having the desire and the physical ability to perform the movements.
    • There are several sub-types.
  19. Verbal apraxia
    apraxia of speech in childhood – will be discussed in more detail in the Language Disorders lecture.]
  20. Basal ganglia
    • a group of cell bodies below cortex interconnected with the cortex, thalamus and brainstem that is involved in motor control and also cognition, emotions, and learning
    • circuitry includes ‘direct’/excitatory and ‘indirect’/inhibitory pathways.
  21. Dopamine
    • a neurotransmitter that plays a key role in the basal ganglia motor circuit and the inhibitory and excitatory pathways.
    • (It is also a key neurotransmitter in the arousal and reward systems.)
  22. Hypokinetic
    characterized by decreased movement
  23. Hyperkinetic
    characterized by increased movement
  24. Parkinson's disease (define, describe cause and treatments)
    • a hypokinetic disease characterized by slowing or loss of movement (akinesia), muscle rigidity, and a ‘pill-rolling’ tremor at rest
    • Cause: due to a loss of dopamine neurons in the basal ganglia that causes a decrease in activity in basal ganglia’s excitatory ‘direct’ pathway
    • Treatments: include medication (L-Dopa), Fetal neural tissue graft, deep brain stimulation (DBS)
  25. Huntington's chorea (define, describe cause and treatments)
    • a hyperkinetic disease characterized by (this is what was written (?))
    • Cause: an autosomal dominant genetic mutation that causes proteins to build up in and ultimately kill cortical neurons (especially in the inhibitory ‘indirect’ pathway of basal ganglia). This cell death is progressive and causes a decline in mental abilities (personality changes, memory issues, dementia) and uncoordinated, jerky body movements (chorea), and eventually leads to death (usually from malnutrition due to constant movement or other complications like pneumonia)
    • Treatments: genetic testing can identify disease risk (if you have the genetic mutation, you will get the disease); medications for symptoms (that reduce neural signaling); nutrition management; physical therapy)
  26. Hemiballismus
    • a relatively rare hyperkinetic disorder characterized by involuntary flinging motions of the extremities that increase with increased activity. Symptoms stop during sleep.
    • Causes: due to damage of the inhibitory pathway of the motor loop, especially from damage to the subthalamic nucleus
    • Treatments: Deep brain stimulation, surgery to remove more basal ganglia, drugs (that reduce neural signaling)
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jocelyn0399
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N165: Quiz 3; Unit 3b
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