2. Programming and Control of Voluntary Movement: Motor Cortex Flashcards

1
Q

multiple cortical motor areas

A
  • 4 areas for movement of limbs and body
  • 2 areas for movement of eyes
  • 1 area for speech (Broca’s area)
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2
Q

4 areas for movement of limbs and body

A
  1. primary motor cortex (area 4)
  2. dorsal premotor cortex (area 6)
  3. ventral premotor cortex (area 6)
  4. supplementary motor area (SMA; area 6)
    - all areas are interconnected (all project and receive projections to/from each other)
    - all receive thalamic input (from basal ganglia and cerebellum with a relay in thalamus)
    - all contribute axons to the corticospinal or pyramidal tract, which means that all can participate in initiation of movement
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3
Q

area 4

A
  • cytoarchitectonically (fine structure) distinct, Betz cells
  • important in control of hands and fingers (fine motor control)
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4
Q

Fritsch and Hitzig

A
  • classic experiments
  • electrical stimulation of motor cortex - brief contraction of one or few muscles on contralateral side of body, somatotropic organization (electrical stimulation will cause AP in neurons)
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5
Q

Wilder Penfield

A
  • tried to find “seizure focus” on epilepsy patients in order to remove it surgically but limit surgical removal to spare language, etc.
  • patients stay awake and able to report experiences
  • confirmation of animal work: distorted map of contralateral body musculature
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6
Q

map in motor cortex

A
  • enlarged representation of parts of the body with more finely controlled or skilled movement (more corticoneurons sent for fine movement)
  • map is not discrete representation of single muscles
  • axons descend on same side of brain until they cross (“decussate”) in the medulla
  • when on opposite side of brain, descending axons are in corticospinal or pyramidal tract
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7
Q

lesions of motor cortex

A
  • decorticate rigidity/spasticity (descending control of stretch reflex)
  • loss of ability to generate independent finger movements
  • recovery of voluntary movement greater in legs than hand and arm (not permanent paralysis) - other regions must be able to issue commands for movement
  • NOT paralysis (spinal cord damage), involuntary movements (damage to basal ganglia), ataxic movements (damage to cerebellum - uncoordinated movements)
  • typically from injury and not from diseases (except ALS)
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8
Q

plasticity in cortical maps

A
  • there is a lot of plasticity in cortical organization
  • increased use can result in reorganization, this is true for all areas both sensory and motor
  • new PT techniques to facilitate reorganization
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9
Q

premotor cortex and SMA

A
  • ventral and dorsal premotor cortex (area 6): use sensory info in ongoing control of movement
  • SMA: motor planning, bimanual coordination
  • SMA and apraxia (skilled movement, use of tools)
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10
Q

idea of bimanual coordination

A

2 hands work together but do different movements (like cutting paper, one hand cuts the other holds paper)
- damage more or less localized to SMA and cognitively intact could not demonstrate use of tools (toothbrush, scissors)

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11
Q

3 types of movement as evidence for role of SMA in motor planning

A
  • simple movement (motor cortex, somatic sensory cortex)
  • complex movement (supplementary motor area, motor cortex, somatic sensory cortex)
  • “mental rehearsal” of complex movement (supplementary motor area)
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12
Q

ALS (amyotrophic lateral sclerosis)

A
  • 40s-50s, more common in men
  • rare frequency
  • cause not known, 10% genetic, familial form
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13
Q

symptoms of ALS

A
  • primarily affect motor system (NOT sensory, cognitive or affective)
  • gradual loss of motor control
  • death by respiratory failure
  • 3-5 year survival rate after diagnosis
  • eye movements persist (motoneurons for extraocular muscles, CN III, IV, VI do not degenerate)
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14
Q

CNS in ALS

A
  • very specific cell populations and fiber tracts are affected: neurons in motor cortex whose axons descend to spinal cord (upper motoneurons) and spinal (lower) motoneurons die.
  • when a neuron dies, its axon dies so the corticospinal tract degenerates
  • motoneurons in CNN nuclei 3,4,6 work; some effects on mn in 5,7,9,10,12
  • gammaMNs do not degenerate, only alpha
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15
Q

what happens to corticospinal axons in ALS

A
  • corticospinal axons die and are replaced by scar tissue –> sclerosis
  • corticospinal axons are lateral in the spinal cord
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16
Q

treatment of ALS

A
  • no cure, supportive care only