Corticospinal and Corticobulbar Fibers Flashcards

1
Q

describe the output of the primary motor cortex

A
  • pyramidal cells in layer 5 (internal pyramidal layer) communicate directly or indirectly (via interneurons) with lower motor neurons
    • corticobulbar fibers project to brainstem
    • corticospinal fibers project to spinal cord
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2
Q

describe inputs to the primary motor cortex

A
  • primary somatosensory cortex
    • Brodmann’s areas 3, 1, 2
  • premotor areas: programmed responses to sneosry input or plans
  • posterior parietal cortex (Brodmann’s areas 5 and 7) integrates sensory info. for motor planning in concert with premotor areas
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3
Q

describe subcortical influences on motor cortex

A
  • the main function of the corticospinal and corticobulbar tracts is voluntary contraction and relaxation of muscles
  • sensory input from the periphery is processed by the cortex, which constantly modifies the signals transmitted through these tracts
  • inputs to the cortex from the basal ganglia and cerebellum via the thalamus also modulate corticospinal and corticobulbar output
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4
Q

describe the roles of the primary and premotor cortices

A
  • with repeated flexion/extension of a finger, discrete areas of the primary motor cortex and primary somatosensory cortex are active
  • as sequenced movements become more complex, the medial premotor area becomes increasingly active
  • during mental rehearsal, only the supplementary motor area is active, indicating that it has been functionally disconnected from the primary motor area
  • lateral premotor areas are move involved in movement under sensory guidance
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5
Q

describe the actions that take place in these brain regions

A
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6
Q
A
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7
Q

describe the route of the corticospinal tract

A
  • cortex
  • corona radiata
  • internal capsule - posterior limb
  • crus cerebri
  • basilar pons
  • pyramid (medulla)
  • pyramidal decussation
  • corticospinal tracts in spinal cord
  • syanpses on alpha and gamma motor neurons in spinal ventral horn
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8
Q

contrast the lateral and anterior corticospinal tracts

A
  • the overwhelming bulk of the corticospinal fibers cross to the opposite side of the nervous system (decussate) in the caudal medulla to form the lateral corticospinal tract (part of the lateral column of spinal white matter), whereas residual uncrossed fibers form the clinically less significant anterior corticospinal tract
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9
Q

describe damage to the corticospinal fibers rostral vs caudal to pyramidal decussation

A
  • damage to the corticospinal fibers rostral to the pyramidal decussation produces contralateral paresis
  • damage to the lateral corticospinal tract caudal to the decussation produces ipsilateral paresis
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10
Q
A
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11
Q

describe upper motor neuron lesion signs

A
  • hyperreflexia
  • extensor plantar response (Babinski reflex)
  • clonus
  • shock (with bilateral damage)
    • first flaccid paralysis (similar to LMN lesion), later spastic paralysis
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12
Q

describe lower motor neuron lesions

A

signs ipsilateral to lesion, example is ALS

  • hyporeflexia
  • hypotonia
  • fasciculations
  • fibrillations
  • profound atrophy/wasting
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13
Q

describe motor manifestations of Brown-Sequard syndrome

A
  • at the level of the lesion, there is also damage to the LMN
    • hyporeflexia
    • wasting of muscles
    • flaccid paralysis
    • fasciculations
    • fibrillations
  • below the lesion, an UMN lesion syndrome occurs ipsilaterally
    • hyperreflexia
    • clonus extensor plantar reflex
    • spastic paralysis
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14
Q

describe manifestations of paraplegia

A
  • transient flaccid paralysis below the level of the lesion (related to spinal shock) followed later by persistent spasticity
  • increased deep tendon reflexes and clonus
  • extensor plantar response (Babinski sign)
  • early transient retention of urine with painless distension of the bladder and overflow (reflex emptying may return with passage of spinal shock)
  • paraplegia in flexion
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15
Q

describe how an infarction of the internal capsule affects the hypoglossal nucleus

A
  • damage to corticobulbar fibers that project to the hypoglossal nucleus causes a contralateral deviation of the tongue during protrusion
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16
Q

describe how an infarction to the internal capsule affects the PPRF

A
  • damage to the corticobulbar fibers projecting to the contralateral PPRF in the caudal pons causes a deviation of both eyes towards the lesion
  • the PPRFs receive bilaterally equal tonic innervation which makes it possible to look straight forward
    • if the innervation of one PPRF is lost, the tonic innervation of the other side is unopposed, causing deviation of the eyes towards the side of the damaged upper motor neurons
17
Q

describe a central (cortical) facial lesion

A
  • the facial nucleus is subdivided into upper and lower facial nuclei
    • the upper facial nucleus receives bilateral innervation through corticobulbar fibers from the ventrolateral primary motor cortex
    • the lower facial nucleus receives only contralateral projections
  • therefore, in a unilateral corticobulbar lesion, the patient is still able to wrinkle the forehead, while a lesion affecting the faical nerve, both upper and lower facial muscles are paralyzed (Bell’s palsy)
18
Q

describe what happens during an UMN facial lesion

A
19
Q

describe what happens during a LMN facial lesion (peripheral)

A