Cortex & Movement Flashcards

1
Q

What are the predominate neurotransmitters for LMN and UMN?

A

LMN: ACh
UMN: glutamate

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2
Q

What are the major cortical UMN tracts?

A

Corticospinal to spinal nerve LMN, corticobulbar to cranial nerve LMN

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3
Q

What are the brainstem UMNs?

A

Eye movement: sup colliculus vergence center

Vestibular nuclei, red nucleus, reticular formation nuclei

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4
Q

What are the 2 cortical UMN areas?

A

Primary motor cortex for focal m contractions, and premotor cortex for planning/sequencing of patterned movements

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5
Q

Describe modulation of the primary motor cortex.

A

Premotor cortex to plan, somatosensory cortex to integrate, thalamus VPM/VPL somatosensory and VL/VA motor

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6
Q

What is motor apraxia?

A

Lesion to premotor cortex or parietal lobe, inability to perform a planned movement w/o paralysis or ataxia

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7
Q

What are the neurons of empathy?

A

Mirror neurons in premotor cortex

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8
Q

What are the 2 modulators of motor thalamus?

A

Basal nuclei (internal globus pallid us, ipsilateral) and pontocerebellum (coordinating intended movement; contralateral)

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9
Q

What are the locations and functions of lateral and medial premotor cortex?

A

Lat: planning/sequencing of grasping movements, front precentral gyrus, visual/verbal guide
Med: supp motor area, planning/sequencing of complex movements, bilateral effects, post-medial part sup frontal gyrus

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10
Q

Where does corticobulbar tract project?

A

Non-ocular CN LMNs bilaterally. There are no cortical UMN projections to ocular CN motor nuclei.

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11
Q

What are symptoms of unilateral UMN lesions?

A

Little effect on LMN of CN 5, 9, 10, 12. For 7: paralysis of contra lower face, forehead spared

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12
Q

What are LMN signs?

A

Ipsilateral deficit, atonia, atrophy, areflexia, fasciculations

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13
Q

What are UMN signs?

A

Positive: spasticity, clasped knife, hyperreflexia, Babinski, clonus, pronator drift, no muscle wasting
Negative: weakness/paralysis, loss of dexterity

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14
Q

What is the underlying cause of spasticity?

A

Exaggerated m spindle stretch reflexes because of abnormal alpha-gamma activation

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15
Q

What are three proposed mechanisms leading to spasticity?

A

Loss gamma/alpha neuron inhibition, unopposed action certain brainstem pathways, maladaptive remodeling in cord or brain

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16
Q

What is the lentiform nucleus?

A

Putamen and globus pallidus

17
Q

Where in the posterior limb internal capsule are corticobulbar, corticospinal, and thalamocortical fibers located?

A

Bulb: near genu
Spine: posteriorly
TC: face near genu, body posteriorly

18
Q

What part of the crus cerebra is corticospinal and corticobulbar tracts? What’s in the other parts?

A

Middle 3/5
Anterior 1/5: corticopontine fibers from anterior cortex
Posterior/lateral 1/5: corticopontine from posterior cortex

19
Q

What are the three types of brainstem lesions that affect corticospinal and specific CNs? What are these called? What are the symptoms?

A

Alternating hemiplegias: corticospinal tract and CN 3 (midbrain lesion), CST and CN 6 (pontine), CST and CN 12 (medulla)
Symp: LMN lesion on 1 side, UMN on alternate side

20
Q

What is affected by lenticulostriate lacunar capsular stroke?

A

Internal capsule, caudate, putamen, globus pallidus

21
Q

What are symptoms of lesion to posterior limb internal capsule?

A

Contralateral spastic paralysis and loss of conscious somatosensation of body, lower contra face paralysis, contra loss conscious somatosensation face