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Neuro Block 7 > Motor Cortex And Pyramidal Motor System > Flashcards

Motor Cortex And Pyramidal Motor System Flashcards

1
Q

Corticospinal and corticonuclear projections through the corona radiate motor

A

Descend through internal capsule

Descends through cerebral peduncle, basilar pons, pyramids, forms AL corticospinal tracts

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2
Q

What is the order from front to back of the different motor cortex

A
  • frontal eye fields
  • Premotor area and supplementary motor area
  • primary motor
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3
Q

Is the cingulate gyrus motor

A

No

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4
Q

What runs through the pyramid

A

Corticospinal system
Corticonuclear system,
Cortico-pontine projections

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5
Q

Corticonuclear system, UMN projections to:

A

LMN in brainstem

-3-12

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6
Q

Postcentral gyrus map

A

Low extremity: medially

Upper extremity: laterally

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7
Q

Corticospinal system

A
  1. Cerebral peduncle
    2 basilar pons
  2. Pyramid
  3. Pyramidal decussation
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8
Q

Anterior limb of the internal capsule

A

Runs between the caudate nucleus medially and putamen and globus pallidus laterally

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9
Q

Posterior limb of the internal capsule

A

Runs between thalamus medially and putamen and globus pallidus laterally

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10
Q

What does the posterior limb of the internal capsule represent

A

Upper extremity
Trunk
Lower extremity

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11
Q

Where is the face represented on the internal capsule

A

Genu

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12
Q

What kind of info is in the internal capsule

A

Descending

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13
Q

What part of the brainstem does the corticospinal system go through

A

Ventral brainstem

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14
Q

Supplementary motor cortex

A
  • active during sequence of finger flexion
  • active during mental rehearsal of sequencing of finer flexion

Guides motor cortex and planning movements

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15
Q

Premotor cortex function

A

Motor planning

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16
Q

Input to premotor cortex

A

Mostly sensory info

  • proprioception from primary somatosensory cortex
  • body awareness from 2ndry somatosensory cortex
  • motor related nuclei of the thalamus
  • complex spatial posteiror parietal cortex
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17
Q

Projections from premotor cortex

A

To primary motor cortex, anteiror horn, reticulospinal system

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18
Q

Deficits in the premotor cortex

A

Apraxia

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19
Q

Impairment in complex movements or sequences of movements, especially learned movements

A

Apraxia

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20
Q

When the premotor cortex is damaged

A

Selective damage does NOT produce significant weakness or paralysis

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21
Q

Supplementary cortex function

A

Motor planning and execution

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22
Q

Input to the supplementary cortex

A

Motor prefrontal and parietal association cortex

  • visual and somatosensory info from parietal association cortex
  • prefrontal input probably related to learned movements
  • motor related nuclei of the thalamus-motor coordination by cerebro-cerebellum system and basal ganglia
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23
Q

Projections of the supplementary cortex

A

To primary motor cortex, anterior horn, reticulospinal system

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24
Q

Deficits when the supplementary cortex is damaged

A

Apraxia

25
Q

Where are the frontal eye fields

A

Overlaps with the premotor cortex in middle frontal gyrus

26
Q

Where do the frontal eye fields project to

A

Tract of nuclei of CN 3, 4, 6 to mediate voluntary eye movement in all directions

27
Q

Circuit for voluntary conjugate eye movements: UMN are in the frontal eye field

A

-FEF corticonuclear projections are bilateral to CN3 and CN6 nuclei. FEF corticonuclear projections are unilateral to contralteral abducens nucleus. FEF drives lateral conjugate gaze toward opposite side: left FEF=right ward gaze. So, unilateral FEF damage causes eyes to deviate toward the lesioned size. Left FEF lesion=left ward deviation

28
Q

How do frontal eye fields drive lateral gaze

A

Opposite side: left FEF=right-ward gaze

29
Q

Unilateral FEF damage

A

Causes eyes to deviate toward the lesioned side

Left FEF lesion=left ward deviation

30
Q

If there is a problem with FEF how can the eyes still move laterally?

A

VOR reflex

31
Q

Voluntary suppression of urinary voiding

A

Cortical micturition center
Prefrontal cortex inhibits the brainstem pathway that promotes voiding. Neurons in the midline part of the superior frontal gyrus send descending excitatory projections to brainstem interneurons, whihc then inhibit the pontine micturition center.

32
Q

Frontal type incontinence

A
  • bilateral damage causes incontinence
  • unilateral damage effects are variable, some weakness/incontinence can occur
  • inability to stop urination, complete reflex voiding occurs
  • may also lack awareness of deficit and emotional reaction to it
  • all reflex voiding mechanisms are intact, so absence of (detrusor-sphincter days-synergia, urge incontinence, incomplete voiding)
33
Q

What is responsible for urinary storage?

A

Sympathetic NS

Inhibits de trusts
Activates internal sphincter

34
Q

MCA infarct would affect what

A

All structures in the motor cortex all the way to the distal arm

35
Q

MCA superior division territory deficits

A

Premotor cortex: apraxia
Frontal eye field: gaze deviation
Broca’s area: language output

36
Q

What supplies the dorsolatral parts of frontal, parietal, and cingulate gyrus

A

ACA

37
Q

What is the cingulate gyrus supplied by

A

Pericallosal branch of ACA

38
Q

What is the superior frontal gyrus supplied by

A

Callosomarginal branch of ACA

39
Q

Callosomarginal branch occlusion

A

Leg portion of primary motor cortex, entire supplementary motor cortex, cortical micturition center

40
Q

What are some areas that are possible sites of disruption due to a watershed

A

Premotor cortex (MCA superior territory), supplementary motor cortex (ACA territory), micturition inhibitory area (ACA territory), frontal eye fields (MCA superior territory)

41
Q

Unilateral ACA stem occlusion

A

-left distal ACA “steals” collateral flow from the right ACA
-potentially insufficient cerebral blood flow through both ACAs
-potentially bilateral deficits, more severe on side of occlusion
-f/u: unilateral deficits due to infarct on the side of occlusion, non-occluded side recovers, deficits resolve.
Can have frontal type incontinence

42
Q

ACA-MCA watershed territory infarcts motor system deficits

A
  • primary motor: variable outcome-hip, trunk, proximal arm weakness
  • premotor: apraxia, unless primary cortex also damaged (weakness masks it)
  • FEF: voluntary lateral age deficits, ipsilateral deviation of forward gaze
43
Q

Primary motor cortex deficit

A

Spastic paresis/paralysis

44
Q

Premotor cortex deficit

A

Apraxia, bu not weakness (if primary is spared)

45
Q

Supplementary motor cortex deficit

A

Apraxia but no weakenss ( if primary is spared)

46
Q

Frontal eye field deficit

A

Horizontal gaze palsy, eyes deviant toward lesioned side

47
Q

Brock’s areadeficit

A

Brocas aphasia

48
Q

When could you see frontal type incontinence

A

Bilateral damage to MCA

49
Q

What is the internal capsule blood supply

A

Lenticolostriate arteries and anterior choroidal artery

50
Q

Lesion to the right internal capsule or complete unilateral damage to right corticospinal tracts in brainstem

A
  • hemiplegic gait
  • lower face weakness in ipsilateral side of hemiplegia
  • slight head deviation due to weak sternocleidomastoid
51
Q

Patient compensates for weakness in leg by using trunk postural movements to passively swing the affected leg around to a forward position

A

Hemiplegic gait

52
Q

Danger of growing intracranial mass

A

Herniated can induce reflex posturing in unconscious patients

53
Q

Decortate (flexor-extensor) posturing/rigidity in unconscious patient

A

Supratentorial mass abolishes cortical suppression of reflex posturing

  • midbrain projections to spinal cord LMNs mediate tonic arm flexion, enhanced by cerebellar influence on midbrain
  • this gets knocked out
54
Q

Decerebrate (extensor) posturing/rigidity

A
  • trans-tentorial mass or herniation compresses midbrain and suppresses the midbrain arm flexion pathway
  • descending extensor systems are still intact
55
Q

What kind of disorder is cerebral palsy

A

Acquired, congenital

56
Q

Distribution of cerebral palsy

A

Diffuse

57
Q

What is cerebral palsy cause by

A

Transient hypoxia/ischemia at birth

Other possibilities are intracranial hemorrhage, CNS viral infection

58
Q

Hallmark presentation of cerebral palsy

A
  • variable degree of weakness and impaired motor coordination
  • increased muscle tone in some muscles-typically hyper-flexion
  • reduced muscle tone and movement
  • dyskinetic: involuntary movements
59
Q

ALS

A

UMN and LMN neurodegeneration

Neuro Block 7 (10 decks)

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