Cortical control of movement Flashcards

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1
Q

location of primary motor cortex

A

precentral gyrus - brodmann’s #4

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2
Q

organization of primary motor cortex

A

similar to homonculus for sensory cortex
cells that control the LE are primarily on the medial side of cortex
cells that control the UE and face are primarily are on the lateral side of the cortex

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3
Q

function of primary motor cortex

A

execution of movement. Here is a more specific breakdown from the notes:

initiates and executes voluntary skilled complex movements
regulates force, direction, and speed of complex movements
isolates joint movement – i.e. FRACTIONATION
produces synergistic actions by activating multiple muscle groups and or movements at multiple joints at once
controls reciprocal movements by simultaneously activating a muscle while inhibiting the antagonist
mediates muscle co contraction (when agonists and antagonists need to contract together)
contributes to the establishment of postural stability required in anticipation of voluntary movements

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4
Q

s/s associated with lesions in primary motor cortex

A

S/S will be contralateral to lesion
Affected portion of body will be determined by the location of the lesion in the cortex
lateral cortex = UE and face
medial cortex = LE

S/S include UMN syndrome s/s:

  • weakness (paresis)
  • spasticity (usually)
  • no early atrophy (muscles may atrophy months later due to disuse)
  • abnormal reflex activity (Babinski reflex, clonus)
  • hyperreflexia
  • decreased coordination
  • abnormal muscle recruitment
  • decreased muscular endurance
  • loss of fractionation producing abnormal muscle synergies
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5
Q

what arteries supply the primary motor cortex and what do disruptions in each cause

A

medial portion of the cortex = ACA
disruption will affect LE

lateral portion of the cortex = MCA
disruption will affect UE

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6
Q

under what circumstances do lesions in the cortex produce exceptions to the rule that UMNs produce spasticity

A

may INITIALLY have flaccid paralysis due to cerebral shock for about 1 week
however this often will convert to spasticity after the period of cerebral shock

may occasionally see long term hypotonia if the lesion is very extensive

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7
Q

where is the supplementary cortex located and what arteries supply it

A

Broadmans area 6, medial aspect of cortex
immediately anterior to #4
supplied by ACA

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8
Q

2 main functions of supplementary motor cortex

A

planning internally guided movement that are goal oriented or complex sequences
that is, movement not guided by visual or auditory cues

also helps to control bimanual tasks

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9
Q

lesions in supplementary cortex produce what s/s

A

ideomotor apraxia

difficulty with tasks requiring coordination of hands and feet

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10
Q

where is the premotor cortex located and what artery supplies it

A

Broadmans area 6, lateral aspect of cortex

Supplied by MCA

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11
Q

function of premotor cortex and how does it differentiate from supplementary

A

the premotor cortex plans movements that are guided externally
i.e. ones that require sensory guidance

this is different from the supplementary motor cortex which plans movements that do not require external stimuli

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12
Q

deficits associated with lesion in premotor cortex

A

ideomotor apraxia when performing an action that relies on sensory stimuli

impaired bimanual coordination

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13
Q

location/arteries of posterior parietal cortex

A

Broadmans areas 5 & 7

supplied by MCA (primarily) and PCA

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14
Q

location/arteries of primary sensory area

A

Broadmans areas 3, 1, & 2 on the postcentral gyrus

supplied by MCA (lateral cortex) and ACA (medial cortex)

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15
Q

motor deficits associated with a lesion in posterior parietal cortex

A

ideomotor apraxia, similar to that seen in the premotor cortex

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16
Q

motor deficits associated with a lesion in primary sensory area

A

contralateral sensory motor ataxia (impairment of coordination)
contralateral impaired grip and load force synergies
impaired balance

17
Q

function of cingulate cortex

A

movement execution during complex behaviors and emotional control of movement

18
Q

function of prefrontal cortex

A

motor memory and motor learning

19
Q

function of frontal eye fields

A

activates eyes to look to contralateral side
i.e. left frontal eye field moves eyes to the right
important note: frontal eye fields (motor involvement) are located in the frontal lobe, NOT the occipital lobe where the primary visual cortex (sensory involvement) is
if there is a lesion here, eyes will drift to the side of the lesion - this is because such a lesion here will interrupt the innervation that moves the eyes to the opposite side and thus those muscles simply remain inactive

20
Q

where are the cell bodies whose axons form the corticospinal-corticobulbar pathway located

A
primary motor cortex - most lateral portion where the face is represented 
premotor cortex
supplementary area
primary sensory cortex
frontal eye field
21
Q

where do the cell bodies whose axons form the corticospinal-corticobulbar pathway terminate

A

alpha motor neurons, gamma motor neurons, and interneurons (highest density)
cranial nerve motor nuclei - corticobulbar
ventral horn of the spinal cord - corticospinal

22
Q

what is a brown-sequard lesion and what motor deficits are associated with it

A

Lesion in half of the spinal cord
Ipsilateral LMN symptoms at site of lesion
Ipsilateral UMN symptoms below site of lesion

23
Q

mixed UMN and LMN and vestibulospinal lesions in the spinal cord

A

Alpha or LMN: hypotonia, early atrophy, hyporeflexia, weakness to muscles at the lesion on ipsilateral side

Lateral corticospinal tract: ipsilateral UMN symptoms below the lesion

Lateral vestibulospinal tract: ipsilateral LMN symptoms below the lesion