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BOARD Review > Ch. 6 One-liners > Flashcards

Ch. 6 One-liners Flashcards

1
Q

Function of the lateral cortico-spinal tract

A

Motor

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2
Q

Function of the posterior columns

A

Sensory (vibration, propriosension, fine touch)

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3
Q

Function of anterolateral pathway

A

Sensory (pain, temperature, crude touch)

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4
Q

Sulcus that divides the frontal obe from the parietal lobe

A

Central/Rolandic sulcus

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5
Q

Location of primary motor cortex

A

precentral gyrus (Brodmann’s 4)

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6
Q

Location of primary somatosensory cortex

A

postcentral gyrus (Brodmann’s 3, 1, 2)

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7
Q

brodmann’s area for primary motor cortex

A

four

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8
Q

brodmann’s areas for primary somatosensory cortex

A

3, 1, and 2

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9
Q

Lesions in the primary motor and primary somatosensory cortex cause what deficits?

A

motor or sensory deficits, respectively, in the contralateral body

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10
Q

Location of premotor cortex

A

just anterior to the primary motor cortex (Brodmann’s 6); (laterally)

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11
Q

Location of the suuplementary motor area

A

just anterior to the primary motor cortex (Brodmann’s 6) (medially)

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12
Q

Function of premotor cortex and supplementary motor areas

A

higher-order motor planning

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13
Q

Location of parietal association cortex

A

parietal lobe posterior to primary somatosensory cortex, superior parietal lobule (Brodmann’s 5, 7)

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14
Q

Location of Secondary somatosensory area

A

Parietal operculum (posterior to primary somatosensory cortex, laterally)

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15
Q

Function of somatoesosory association cortex

A

higher-order sonsory processing

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16
Q

Lesions in the sensory or motor association cortex cause what deficits?

A

higher-order sensory analysis or motor planning

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17
Q

How is the cortex organized?

A

somatotopically, depicted by the humunculus

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18
Q

What is the somatotopic respresentation?

A

arms medial to legs with two exceptions: primary sensorimotor cortices and posterior columns

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19
Q

Where are sensory neurons located?

A

dorsal root ganglia

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20
Q

Where do axons from sensory neurons travel?

A

bifurcate - conveying sensory info from the periphery, through spinal nerve, and carreis through dorsal root filaments, to dorsal horn

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21
Q

What is the dorsal horn for?

A

sensory processing

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22
Q

What is the ventral horn for?

A

contains motor neurons

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23
Q

Where do motor neurons send their axons

A

located in the ventral horn, axons are sent through the ventral root filaments to the periphery

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24
Q

What are the nuclei of the dorsal horn?

A 
Marginal zone
Substantia gelatinosa
nucleus proprius
Neck of dorsal horn
Base of dorsal dorn
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25
Q

What is contained within the intermediate zone?

A

interneurons and certain specialized nuclei

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26
Q

What are the nuclei of the intermediate zone?

A

Clarke’s nucleus, intermediolateral nucleus

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27
Q

What are the nuclei of the ventral horn?

A

Medial motor nucleus
Commissural nucleus
Lateral motor nucleus

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28
Q

What is the nuclei in the gray matter surrounding the central canal?

A

Grisea centralis

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29
Q

What Bror Rexed Laminae is represented by the marginal zone?

A

I

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30
Q

What Bror Rexed Laminae is represented by the substantia gelatinosa?

A

II

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31
Q

What Bror Rexed Laminae is represented by the nucleus proprius?

A

III and IV

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32
Q

What Bror Rexed Laminae is represented by the neck of the dorsal horn

A

V

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33
Q

What Bror Rexed Laminae is represented by the base of the dorsal horn?

A

VI

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34
Q

What Bror Rexed Laminae is represented by The intermediate zone (Clarke’s nucleus and intermediolateral nucleus?

A

VII

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35
Q

What Bror Rexed Laminae is represented by the commissural nucleus

A

VIII

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36
Q

What Bror Rexed Laminae is represented by The medial and lateral motor nuclei?

A

IX

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37
Q

What Bror Rexed Laminae is represented by the grisea centralis?

A

X

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38
Q

columns of white matter in spinal cord

A

dorsal (posterior), lateral, and ventral (anterior) columns

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39
Q

where is white matter the thickest in the spinal cord

A

cervical levels where most ascending fibers have entered and more descending fibers have not terminated

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40
Q

where is there more gray matter in the spinal cord

A

cerival and lumbosacral, esp. in ventral horn due to nerve plexuses for arms and legs

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41
Q

where is the intermediolateral cell column

A

lateral horn in thoracic cord

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42
Q

What characterizes the sacral cord?

A

mostly gray matter

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43
Q

What characterizes the cervical cord?

A

white matter is the thickest

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44
Q

What characterizes the thoracic cord?

A

lateral horn containing intermediolateral cell column

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45
Q

What is the cervical enlargement?

A

gives rise to the nerve plexus for the arms

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46
Q

What is the lumbosacral enlargement?

A

gives rise to the nerve plexus for the legs

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47
Q

Spinal levels of cervical enlargement

A

C1-T3

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48
Q

Spinal levels of lumbosacral enlargement?

A

L1-S2

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49
Q

What is the blood supply to the spinal cord?

A

anterior and posterior spinal arteries forming the spinal arterial plexus, and radicular arteries

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50
Q

What gives rise to the anterior spinal artery?

A

Vertebral arteries

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51
Q

What does the anterior spinal artery supply?

A

anterior 2/3rds of cord (anterior horns and anterior and lateral white matter columns)

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52
Q

What gives rise to the posterior spinal artery?

A

posterior inferior cerebellar artery (PICA) and vertebral arteries

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53
Q

What does the posterior spinal artery supply?

A

posterior 1/3 of the cord (posterior columns and part of posterior horns)

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54
Q

Describe the involvement of the aorta in blood supply to the cord?

A

gives rise to 31 segmental branches that enter the spinal canal; most supply the meninges; 6-10 reach the spinal cord as radicular arteries

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55
Q

What gives rise to radicular arteries and how many are there?

A

aorta, 6-10

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56
Q

What is the great radicular artery of Adamkiewicz?

A

a prominent radicular artery that is major blood supply to the lumbar and sacral cord

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57
Q

Spinal level of great radicular artery of Adamkiewicz?

A

usually b/w T9-T12; but can be anywhere b/w T5-L3

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58
Q

What is the vulnerable zone of the cord?

A

an area of relatively decreased perfusion between the lumbar and vertebral arterial supplies; located in mid-thoracic region at about T4-T8

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59
Q

Where is the vulnerable zone located?

A

mid-thoracic; T4-T8

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60
Q

What is the significance of the vulnerable zone?

A

susceptible to infarct during thoracic surgery or conditions that cause decreased aortic pressure

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61
Q

What is the venous drainage of the spinal cord?

A

Batson’s plexus - a plexus of veins in the epidural space

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62
Q

Explain how metastatic cells from prostate cancer or a pelvic infection might enter the epidural space?

A

the epidural veins of Batson’s plexus don’t contain valves, allowing reflux of blood with increased intra-abdominal pressure

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63
Q

What is apraxia? Lesions where may cause it?

A

deficit in higher-order motor planning and execution despite normal strength;
caused by lesions in association areas

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64
Q

Where are upper motor neurons located?

A

cerebral cortex

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65
Q

Where are lower motor neurons located?

A

spinal cord and brainstem

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66
Q

Where are lateral motor systems located in the spinal cord?

A

travel in lateral columns, synapse on lateral ventral horn motor neurons and interneurons

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67
Q

Where are medial motor systems located in the spinal cord?

A

travel in anteromedial spinal cord, synapse on the medial ventral horn motor neurons or interneurons

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68
Q

What tracts carry the lateral motor systems?

A

lateral corticospinal tract and rubrospinal tract

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69
Q

Function of lateral corticospinal tract

A

movement of contralateral limbs (esp. rapid, dextrous movements of individual digits or joints)

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70
Q

What is the site of origin of the lateral corticospinal tract?

A

primary motor cortex (Brodmann’s 4) (over 50% of fibers), preotor and supplementary motor areas (area 6), or parietal lobe (areas 3, 1, 2, 5, 7)

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71
Q

Where does the lateral corticospinal tract decussate?

A

pyramidal decussation, at the cervicomedullary junction

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72
Q

Termination of lateral corticospinal tract

A

Entire cord (predominantly at cervical and lumbosacral enlargements)

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73
Q

What is the most clinically important motor tract?

A

lateral corticospinal tract

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74
Q

Function of rubrospinal tract

A

movement of contralateral limbs
taking over after cotricospinal injury
flexor posturing of upper extremity
seen in lesions above red nuclei when it is spared

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75
Q

Origin of rubrospinal tract

A

Red nucleus, magnocellular division

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76
Q

Termination of rubrospinal tract

A

cervical cord

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77
Q

Decussation of rubrospinal tract

A

ventral tegmental decussation, in midbrain

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78
Q

What tracts are involved with the medial motor system?

A

anterior corticospinal tract
medial and lateral vestibulospinal tracts
reticulospinal tracts
tectospinal tracts

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79
Q

Function of anterior corticospinal tract

A

contraol of bilateral axial and girdle muscles (postural tone and balance)

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80
Q

Function of medial VST

A

positioning of head and neck

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81
Q

Function of lateral VST

A

balance

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82
Q

Termination level of medial VST

A

cervical and upper thoracic cord

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83
Q

Termination level of lateral VST

A

entire cord

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84
Q

Origin of anterior corticospinal tract

A

primary motor cortex and supplementary motor area

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85
Q

Origin of medial VST

A

medial and inferior vestibular nuclei

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86
Q

Origin of lateral VST

A

lateral vestibular nucleus

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87
Q

Function of reticulospinal tracts

A

automatic posture and gait-related movements

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88
Q

Origine of reticulospinal tracts

A

pontine and medullary reticular formation

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89
Q

Termination level of reticulospinal tracts

A

entire cord

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90
Q

Function of tectospinal tract

A

coordination of head and eye movement

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91
Q

Origin of tectospinal tract

A

superior colliculus

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92
Q

Decussation of tectospinal tract

A

dorsal tegmental decussation, in midbrain

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93
Q

Decussation of anterior corticospinal tract

A

n/a

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94
Q

Decussation of vestibulospinal tracts

A

n/a

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95
Q

Decussation of reticulospinal tracts

A

n/a

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96
Q

Explain why a unilateral lesion to the medial motor system causes no obvious deficits?

A

they terminate on interneurons that project to both sides of the psinal cord, controlling mevements that involve bilateral spinal segments

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97
Q

Cortical layer of the lateral croticospinal tract

A

5

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98
Q

Where do layer 5 pyramidal cells synapse

A

directly onto motor neurons in the ventral horn, and spinal interneurons

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99
Q

What are Betz cells

A

the largest neurons in the nervous system, comprise 3% of corticospinal neurons

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100
Q

Where do axons from cerebral cortex of lateral corticospinal tract go

A

upper portion of cerebral white matter (corona radiata), descend toward internal capsule

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101
Q

What does cerebral white matter convey

A

bidirection info btwn different cortical areas, btwn cortex and deep structures (like basal ganglia, thalamus, and brainstem)

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102
Q

location of internal capsule

A

thalmus and caudate nucleus are always medial to and globus pallidus and putamen are always lateral to

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103
Q

three parts of internal capsule

A

anterior limb, posterior limb, genu

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104
Q

anterior limb separates

A

separates head of caudate from the globus pallidus and putamen

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105
Q

posterior limb separates

A

separates thalamus from globus pallidus and putamen

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106
Q

genu location

A

transition from anterior and posterior limbs at the level of the foramen of Monro

107
Q

where is the corticospinal tract in the internal capsule

A

posterior limb

108
Q

corticobulbar fibers

A

project from cortex to brainstem (bulb); contain motor fibers for the face

109
Q

orientation of somatotopic map in corticospinal tract

A

anterior to posterior and medial to lateral: face, arm, trunk, leg

110
Q

What is the effect of a lesion of the lateral corticospinal tract at the level of the internal capsule

A

weakness of the entire contralateral body (face, arm, and leg) despite somatotopic organization, because the fibers are compact; occaionaly can be more selective motor deficits

111
Q

what does the internal capsule continue into

A

midbrain cerebral peduncles

112
Q

What are the parts of the cerebral peduncle

A

substantia nigra and basis pedunculi

113
Q

Where is the white matter contained in the cerebral peduncle

A

basis pedunculi (ventral portion)

114
Q

Where are the corticobulbar and corticospinal tracts located in the midbrain?

A

the middle third of the basis pedunculi

115
Q

What is the somatotopic organization of the corticospinal fibers in the basis pedunculi?

A

medial to lateral: face, arm, trunk, leg

116
Q

What is contained in other portions of the basis pedunculi?

A

primarily corticopontine fibers

117
Q

Describe the path of the corticospinal fibers:

A

cortex (primary, premotor, and supplementary motor cortex) - posterior limb of internal capsule - middle 1/3rd of basis pedunculi in midbrain - basis pontis in ventral pons - medullary pyramids in ventral/rostral medulla-

  • 85% through pyramidal decussation - lateral white matter columns as lateral corticospinal tract - spinal cord central gray matter to synapse onto anterior horn cells
  • 15% to spinal cord ipsilatterally - anterior white matter columns to form the anterior corticospinal tract
118
Q

where do corticospinal fibers travel after basis pedunculi

A

descend through ventral pons forming scattered fascicles on the basis pontis

119
Q

where do the scattered fascicles of the corticospinal tract collect

A

ventral/rostral surface of medulla to form medullary pyramids

120
Q

What is the cervicomedullary junction?

A

transition from medulla to spinal cord

121
Q

What is the level of the cervicomedullary junction?

A

foramen magnum

122
Q

What occurs to corticospinal tract at cervicomedullary jxn

A

85% pyramidal tract fibers cross over in pyramidal decussation to enter lateral white matter columns - forming the lateral corticospinal tract

123
Q

What occurs to remaining 15% of corticospinal fibers

A

continue ipsilaterally without crossing and enter anterior white matter columns

124
Q

What is another name for the corticospinal tract?

A

pyramidal tract (because fibers collect on the medullary pyramids)

125
Q

What is the somatotopic organization of the lateral corticospinal tract?

A

medial to lateral: arms, trunk, leg

126
Q

Where is the lateral corticospinal tract located in the spinal cord?

A

lateral columns

127
Q

Where do lateral corticospinal tract fibers synapse?

A

anterior horn cells (gray matter)

128
Q

How do autonomic efferents differ anatomically from somatic efferents?

A

they have a peripheral synapse located in a ganglion interposed b/w the CNS and effector gland or smooth muscle; as opposed to somatic efferents which project directly from the CNS (anterior horn or cranial nuclei) to skeletal muscle

129
Q

What is the enteric nervous system

A

a third autonomic division consisting of a nerual pleuxus w/in the walls of the gut; controls peristalsis and GI secretions

130
Q

where are preganglionic neurons of the sympathetic division located

A

intermediolateral cell column, in lamina VII (intermediolateral nucleus) of spinal cord levels T1 to L2?3

131
Q

what are the two sets of sympathetic ganglia

A

paired paravertebral sympathetic trunk ganglia (aka sympathetic chain) and unpaired prevertebral ganglia

132
Q

What are the sympathetic chain ganglia from T1-T3?

A

superior, middle (often absent), and iferior/stellate cervical ganglia

133
Q

Where are the prevertebral ganglia located?

A

in the celiac plexus surrounding the aorta

134
Q

What are the prevertebral ganlgia?

A

celiac, superior mesenteric, and inferior mesenteric ganlgia

135
Q

where do parasympathetic preganglionic fibers arise from?

A

cranial nerve parasympathetic nuclei and sacral parasympathetic nuclei

136
Q

Where are the sacral parasympathetic nuclei located?

A

lateral gray matter of S2-S4, in a location similar to the intermediolateral cell column

137
Q

What do sympathetic postganglionic fibers release?

A

norepinephrine; EXCEPTION: sweat glands are Ach

138
Q

What do parasympathetic postganglionic fibers release?

A

acetylcholine

139
Q

What do preganglionic fibers release?

A

acetylcholine

140
Q

What is a treatment for hyperhidrosis and describe the mechanism

A

botulinum toxin - blocks cholinergic receptors, so is injected locally into the skin of the axilla

141
Q

What are signs of LMN injury?

A 
muscle weakness
atrophy
fasciculations
decreased tone
hyporeflexia
142
Q

What are signs of UMN?

A

muscle weakness
spasticity (increased tone and hyperreflexia)
Babinski’s sign
Hoffmann’s sign
Posturing
*mild atrophy may develop after disuse
*acute UMN lesions may initially result in decreased tone and reflexes (flaccid paralysis)

143
Q

What are fasciculations?

A

abnormal muscle twitches caused by spontaneous activity in groups of muscle cells

144
Q

What is spasticity?

A

increased tone and hyperreflexia

145
Q

What is flaccid paralysis?

A

decreased tone and reflexes seen in acute UMN injuries

146
Q

What is an example of an UMN injury causing flaccid paralysis?

A

spinal shock

147
Q

what receptors do parasympathetic postganglionic neurons activate

A

muscarinic cholinergic receptors (M1-3)

148
Q

what receptors do preganglionic neurons activate

A

nicotinic receptors (acetylcholine)

149
Q

what are sympathetic and parasympathetic outflow controlled by

A

directly and indirectly by higher centers like hypothalamus, brainstem nuclei (nucleus soltaris), amygdala, several regions of limbic cortex

150
Q

what else can autonomic responses be regulated by

A

afferent sensory info (chemoreceptors, osmoreceptors, thermoreceptors, baroreceptors)

151
Q

receptors of postganglionic sympathetic neurons

A

alpha 1, alpha 2, beta 1, beta 2, beta 3

152
Q

acute UMN lesion

A

initially flaccid paralysis with decreased tone and reflexes, which gradually change over hours/months into spastic paresis

153
Q

hypothesized mechanism of spasticity

A

caused by damage to descending inhibitory pathways that travel closely with the corticospinal tract, not damage to the spinal tract itself

154
Q

What is Hoffmann’s sign?

A

indicates heightened reflexes involving the finger flexor muscles; loosely hold middle finger, flick fingernail downward causing finger to rebound slightly into extension. If the thumb flexes and adducts in response, Hoffmann’s sign is present

155
Q

What would you name unilateral face, arm, and leg weakness or paralysis?

A

Hemiparesis or hemiplegia; or pure motor hemiparesis

156
Q

Why is the spinal cord ruled out in pure motor hemiparesis?

A

becase the face would be spared with spinal cord lesions

157
Q

Why is pure motor hemiparesis? unlikely to be cortical?

A

the lesion would have to involved the entire strip, in which case sensory involvement in hard to avoid

158
Q

Why is hemiparesis/hemiglegia unlikely to be muscle or peripheral nerve?

A

coincidental involvement of the face, arm and leg, all on one side of the body is unlikely

159
Q

Location of lesion in pure motor hemiparesis

A

corticospinal and corticobulbar tract fibers below the cortex and above the medulla: corona radiate, posterior limb of internal capsule, basis pontis, or middle third of cerebral peduncle

160
Q

What is the side of the lesion in hemiparesis/hemiplegia/pure motor hemiparesis?

A

contralateral (above the pyramidal decussation)

161
Q

What are common causes of pure motor hemiparesis?

A

lacunar infarct of internal capsule or pons, less commonly infarct of cerebral peduncle; demyelination, tumor, or abscess in these location or corona radiata

162
Q

What arteries would be involved with lacunar infarct of the internal capsule?

A

lenticulostriate branches of the middle cerebral artery or anterior choriodal artery

163
Q

What arteries would be involved with lacunar infarct of the pons?

A

median perforating branches of the basilar artery

164
Q

What are associated features of hemiparesis/hemiplegia/pure motor hemiparesis?

A

UMN signs usually present
dysarthria-pure motor hemiparesis
ataxia-hemiparesis

165
Q

What causes ataxia in ataxia-hemiparesis?

A

involvement of the cerebellar pathways (corticopontine fibers)

166
Q

Location of lesion in hemiparesis/hemiplegia associated with somatosensory, oculomotor, viusal, or higher cortical deficits (like aphasia or neglect)

A

Entire primary motor cortex (precentral gyrus), or corticospinal and corticobulbar tract fibers above the medulla

167
Q

Assocaited features of hemiparesis with associated somatosensory, oculomotor, visual, or higher cortical deficits

A

UMN signs usually present
dysarthria possibly
ataxia possibly

168
Q

What is brachiocrural plegia/paresis?

A

hemiplegia/hemiparesis sparing the face; i.e. unilateral arm and leg weakness/paralysis

169
Q

Why wouldn’t brachiocrural plegia/pareses lesions be in the corticospinal tract below the motor cortex above the medulla?

A

The corticobulbar tract is located very close - thus the face would likely be involved

170
Q

Why wouldn’t brachiocrural plegia/paresis be muscle or peripheral nerve lesions?

A

It is unlikely to be coincidental involvement of both the arm and leg on one side of the body

171
Q

Why wouldn’t brachiocrural plegia/paresis lesions be below C5?

A

In that case, some arm muscles would be spared.

172
Q

What are the most likely locations of lesions for brachiocrural plegia/paresis and what side in relation to weakness?

A

arm and leg area of the motor cortex - contralateral
corticospinal tract from lower medulla - contralateral
corticospinal tract in cervical spinal cord (to C5) - ipsilateral

173
Q

Associated features allowing further localization for hemiparesis sparing the face

A

UMNs usually present
Cortical: watershed distribution - proximal more than distal muscles (man in a barrel), aphasia, hemineglect
Medial medullary lesions: loss of vibration and joint position on the same side as weakness, tongue weaness on the opposite side
Extending to lateral medulla: lateral medullary syndrome
Spinal cord: Brown-Sequard syndrome
High cervical: decreased facial sensation due to involvement of spinal trigeminal nucleus and tract

174
Q

Common causes of hemiparesis sparing the face:

A

Watershed infarct (anterior cerebral-middle cerebral watershed)
Medial or combined medial and lateral medullary infarct
MS
Lateral trauma
Compression of the C-spinal cord
Infarcts of the posterior limb of the internal capsule removed from genu (occassionally)

175
Q

What is faciobrachial paresis/plegia?

A

unilateral face and arm wekaness/paralysis

176
Q

Why is a lesion in the internal capsule or below unlikely (but not impossible) in faciobrachial paresis?

A

the corticobulbar and corticospinal tracts are failry compact, resulting in leg involvement

177
Q

Location of lesions involved in faciobrachial paresis/plegia

A

face and arm areas of the primary motor cortex, over the lateral frontal convexity; contralateral

178
Q

Associated features allowing further localization for faciobrachial paresis/plegia

A

UMN usually present
dysarthria usually present
Dominant-hemsphere lesions: Broca’s aphasia common
Nondominant-hemisphere lesions: hemineglect occasionally
Lesion extending into parietal lobe: sensory loss

179
Q

What is the classic cause of faciobrachial paresis/plegia?

A

middle cerebral artery superior division infarct

180
Q

What is another name for unilateral arm weakness or paralysis?

A

brachial monoparesis/monoplegia

181
Q

What is a rare cause of unilateral arm weakness/paralysis?

A

foramen magnum tumors may initially affect one arm

182
Q

Location of lesion in unilateral arm weakness/paralysis

A

contralateral arm area of the primary motor cortex; ipsilateral peripheral nerves supplying the arm

183
Q

Associated features allowing further localization of unilateral arm weakness/paralysis

A

motor cortex: UMN signs, cortical sensory loss, aphasia, subtle invovlement of the face or leg, weakness pattern incompatible with periphal lesion (no sensory loss, proximal strength normal
peripheral lesion: LMN signs, weakness and sensory loss of a known pattern

184
Q

Common causes of unilateral arm weakness/paralysis:

A

motor cortex: infarct of small cortical branch of middle cerebral artery, or small tumor or abscess
peripheral lesion: compression injury, diabetic neuropathy, etc.

185
Q

Crural monoparesis/monoplegia

A

unilateral leg weakness or paralysis

186
Q

Location involved with crural monoparesis/plegia

A

cervical cord tumors rarely - initially cause leg weakness only
contralateral leg area of primary motor cortex (medial surface of frontal lobe)
ipsilateral lateral corticospinal tract below T1
ipsilateral peripheral nerves of leg

187
Q

Associated features allowing localization of crural monoparesis/plegia

A

Motor cortex: UMN signs, cortical sensory loss, frontal lobe signs (grasp reflex) subtle involvement of arm or face, none, weakness pattern incompatible with peripheral (diffuse weakness of on full leg)
Spinal cord: UMN signs, Brown-Sequard syndrome, sensory level, subtle spasicity of contralateral leg, sphincter function involvement, weakness pattern
Peripheral nerve: LMN signs, weakness and sensory loss compatible with known pattern

188
Q

Causes of crural monoparesis/plegia:

A

Motor cortex: anterior cerebral a. infarct; small tumor, abscess etc.
Spinal cord: unilateral cord trauma; compression by tumor; MS
Peripheral nerve: compression injury; diabetic neuropathy etc.

189
Q

Names for unilateral facial weakness/paralysis:

A

Bell’s palsy (peripheral nerve); isolated facial weakness

190
Q

What locations are r/o in unilateral facial weakness/paralysis

A

below the rostral medulla

191
Q

Locations involved in unilateral facial weakness or paralysis:

A

Common: ispilateral peripheral facial nerve (CN VII)
Uncommon: contralateral face area of primary motor cortex or genu of internal capsule (usually arm and leg is involved); facial nucleus and exiting nerve fascicles in the pons or rostral medulla

192
Q

Associated features of unilateral facial weakness/paralysis:

A

Facial nerve: forehead and orbicularis oculi are not spared; hyperacusis, decreased taste, decreased lacrimation, pain behind ear on the affected side
Facial nucleus: forehead and orbicularis oculi are not spared; usually deficits assocaited wth damage to nearby nuclei (VI, V, or corticospinal tract)
rostral lateral medulla: lateral medullary syndrome
Motor cortex or capsular genu: forehead is relatively spared; dysarthria and unilateral tongue weakness are common; subtle arm involvemnt; sensory loss or aphasia

193
Q

What is facial diplegia?

A

bilateral facial weakness; difficult to detect
caused by: motor neuron disease, bilateral peripheral nerve lesions, bilateral white matter abnormalities (ischemia or demyelination)

194
Q

Brachial diplegia

A

bilateral arm weakness

195
Q

Locations involved in brachial diplegia

A

Medial fibers of both lateral corticospinal tracts
B/l cervical spine ventral horns
Peripheral nerve or muscle disorders affecting both arms

196
Q

Associated features in brachial diplegia

A

central or anterior cord syndromes can help localize

197
Q

Common causes of brachial diplegia

A

Central cord syndrome: syingomyelia, intrinsic spinal cord tumor, myelitis
Anterior cord syndrome: anterior spinal artery infarct, trauma, myelitis
Peripheral nerve: b/l carpal tunnel, disc herniation

198
Q

Paraparesis/plegia

A

bilateral leg weakness/paralysis

199
Q

Locations of paraperesis/plegia

A

rarely, cervical cord tumors can initially cause b/l leg weakness w/out involvement of arm
Primary motor cortex b/l leg areas along medial surface of frontal lobes
lateral corticospinal tracts below T1
Causda equina syndrome
Peripheral nerve or muscle disorders

200
Q

Associated localizing features of paraperesis/plegia:

A

B/l medial frontal lesions: UMN signs, frontal lobe dsfxns (confusion, apathy, grasp reflex, incontinence)
Spinal cord lesions: UMN signs, sphincter dsfxn, autonomic dsfxn, sensory level, loss of specific reflexes
Peripheral nerve or muscle disorders:
Cauda equina syndrome ass. w/ sphincter and erectile dsfxn, sensory loss in lumbar or sacral dermatomes, and LMN signs
Symmetrical polyneuropathies: affect distal muscles w/ glove-stocking sensory loss, and LMN signs
Neuromuscular disorders and myopathies: prximal more than distal muscles

201
Q

Causes of paraperesis/plegia

A

spinal cord lesions are a common and serious cause of b/l leg weakness
B/l medial frontal lesions: parasagittal meningioma, b/l anterior cerebral atery infarcts, cerebral palsy (b/l periventricular leukomalacia)
Spinal cord: numerous - tumor, trauma, myelitis, epidural abscess
peripheral nerve or muscle: cauda equina syndrome (tumor, trauma, disc herniation), Guillain-Barre is initially legs, Lamer-Eaton syndrome, distal polyneuropathies

202
Q

Names for bilateral arm and leg weakness or paralysis

A

Quadriparesis, quadriplegia, tetraparesis, tetraplegia

203
Q

Why is the motor cortex below the motor cortex and above the medulla r/o in bilateral arm and leg weakness?

A

face would be involved

204
Q

Why is spinal cord below C5 unlikely in bilateral arm and leg weakness/paralysis?

A

arms would be partly spared

205
Q

Locations involved in bilateral arm and leg weakness/paralysis

A

B/l arm and leg areas of the motor cortex
b/l lesions of corticospinal tracts from lower medulla to C5
peripheral nerve, motor neuron, or muscle disordrs severe enough to affect all limbs usually also affects the face, but may be relatively mild

206
Q

Associated localizing features of quadraparesis/plegia

A

B/l motor cortex lesions: watershed distribution, man in a barrel, UMN signs, aphasia, neglect, cognitive disturbance
b/l upper cervical cord: UMN signs, sensory level, sphincter dsfxn, autonomic dysfxn, respiratory weakness, decreased facial sensation due to involvement of spinal trigeminal nucleus
lower medullary lesions: UMN signs, occipital HA, tongue weakness, sensory loss, hiccups, autonomic dysfxn, sphincter dysfxn, abnormal eye movements
peripheral nerve/muscle: LMN signs

207
Q

Common causes of bilateral arm and leg weakness/paralysis

A

Motor cortex: b/l watershed infarcts (anterior cerebral-middle cerebral watershed
upper C cord and lower medullar lesions: tumor, infarct, trauma, MS
peripheral nerve/muscle: numerous

208
Q

Locations r/o in generalized weakness or paralysis

A

small focal or unilateral lesions

lesions of lower medulla or spinal cord (spare face or UE)

209
Q

Locations involved in generalized weakness or paralysis

A

Bilateral ventral pontine ischemia due to basilar artery stenosis is an important cause of transient generalized weakness
B/l lesions of entire motor cortex
B/l corticospinal and corticobulbar tracts anywhere from corona radiata to pons
Diffuse disorders

210
Q

Associated features allowing localization of generalized weakness

A

UMN vs. LMN signs; sensory loss, eye movement abnormalities, pupillary abnormalities, autonomic disturbances, or impaired consciousness
*Respiratory depression is common with sever generalized weakness

211
Q

Common causes of generalized weakness or paralysis

A

global cerebral anoxia, pontine infarct or hemorrhage (locked-in), amyotrophic lateral sclerosis, Guillain-Barre, myasthenia, botulism, numerous other

212
Q

Spastic gait

A

stiff-leged, circumduction, sometimes with scissoring of the legs and toe-walking (from increased tone in calf muscles), decreased arm swing, unsteady, falling toward side of greater spasticity; can be unilateral or bilateral

213
Q

Localization of spastic gain

A

corticospinal tracts (unilateral or bilateral)

214
Q

Ataxic gait

A

wide based, unsteady, staggering side to side, falling toward side of worse pathology. subtle deficit can be detected with tandem (hell-toe, or “drunk walk”) gait testing

215
Q

Localization of ataxic gait

A

cerebellar vermis or other midline cerebllar structures

216
Q

Vertiginous gait

A

looks similar to ataxic gait: wide based and unsteady. Positive Romberg sign

217
Q

Localization of vertiginous gait

A

vestibular nuclei, vestibular nerve, semicircular canals

218
Q

Frontal gait

A

slow, shuffling, narrow or wide based, “magnetic” (barely raising feet off floor, unsteady. Sometimes resembles Parkinsonian gait. Gait apraxia -can perform cycling mevements on back better than they can walk

219
Q

Localization of frontal gait

A

frontal lobes or frontal subcortical white matter

220
Q

Parkinsonian gait

A

slow, shuffling, narrow based
difficulty initiating walking
stooped forward, decreased arm swing, and “en bloc turning”
unsteady, with “retropulsion,” taking several srapid steps to regain balance when pushed backward

221
Q

Localization of Parkinsonian gait

A

sustantia nigra or other regions of the basal ganglia

222
Q

See table 6.6

A

pg. 251-252 for gait causes

223
Q

Dyskinetic gait

A

dancelike (choreic), glinging (ballistic), or writhing (athetoid) movements with walking, may be accompanied by some unsteadiness

224
Q

Localization of dyskinetic gait

A

subthalamic nucleus, other regions of the basal ganglia

225
Q

Tabetic gait

A

high-stepping, foot flaaping, with particular difficulty walking in the dark or on uneven surfaces; Romberg sign present

226
Q

Localization of Tabetic gait

A

posterior columns or sensory nerve fibers

227
Q

Paretic gait

A

depends on localization of lesion; Trendelnburg gait - waddling with proximal hip weakness; Sudden knee buckling - severe thigh weakness; foot drop can cause a high-stepping, slapping giat, with frequent tripping

228
Q

Localization of paretic gait

A

nerve roots, peripheral nerves, neuromuscular jxn, or muscles

229
Q

Antalgic gait

A

painful; pain may be obvious based on report of facial expression; avoids putting pressure on affected limb

230
Q

Localization of antalgic/painful gait

A

peripheral nerve or orthopedic injury

231
Q

Orthopedic gait disorder

A

depends on nature and location; peripheral nerve injury or spinal cord-related deficits may also be present

232
Q

Localization of orthopedic gait disorder

A

bones, ligaments, tendons, joints, muscles

233
Q

Functional gait disorder

A

hard to dx; reports of poor balance yet sponatneously perfrom highly destabilizing swaying movements while walking, without ever falling

234
Q

Localization of functional gait disorder

A

psycholigically based

235
Q

What is multiple sclerosis?

A

an autoimmune inflammatory disorder affecting CNS myelin, causing slowed conduction velocity, disperios or loss of coherence of action potential volleys, and ultimately conduction block; some axons may also be destroyed in the plaques

236
Q

Why do some patients with MS have worse sx when they are warm?

A

dispersion of action potentials increases with temperature

237
Q

What is the classic clinical definition of MS?

A

Two or more deficits separated in neuroantatomical space and time

238
Q

What are MRI findings of MS?

A

oligoclonal bands, white matter lesions/plaques, T2-bright areas, Dawson’s fingers, acute plaques enhances with gadolinium

239
Q

What are oligoclonal bands?

A

discrete bands on gel electrophoresis resulting from synthesis of large amounts of immnoglobulin by individul plasma cell clones in the CSF

240
Q

What are unusual CSF findings in MS patients? (help r/o MS)

A

> 50 WBCs or with CSF with nonlymphocytes

241
Q

What do T2-bright areas represent in MS patients on MRI?

A

demyelinative plaques in white matter

242
Q

Where are T2-bright areas located in MRI of MS patients?

A

extending into white matter from periventricular locations - resulting in Dawson’s fingers; located in supratentorial and infratentorial structures

243
Q

What are Dawson’s fingers?

A

MS plaques extending into the twhite matter from periventricular locations

244
Q

What can enhance acute plaques in the MRI of MS patients?

A

Gadolinium

245
Q

50% of patients with what sx develop MS?

A

single episode of optic neuritis or transverse myelitits

246
Q

What is the course of MS?

A

relapsing-remitting, but evolves into a more refractory chronic progressive

247
Q

What is the therapy for acute exacerbation of MS?

A

high-dose steroids (speeds recovery but doesn’t effect overall course)

248
Q

What is the first-line therapy for relapsing-remitting MS?

A

beta-IFN and copolymer (glatiramer acetate) - prevent exacerbations and delay progression

249
Q

What are second line treatments for MS?

A

monoclonal antibodies - natalizumab, rituximab, campath

chemotherapeutic agents: cyclophosphamide, mitoxantrone

250
Q

What are motor neuron diseases?

A

disorders, mostly degenerative, that selectively affect UMNs, LMNs or both, producing motor deficits without sensory abnormalities or other findings

251
Q

What is ALS?

A

amyotrophic lateral sclerosis/Lou Gehrig’s disease; progressive degeneration of both upper motor neurons and lower motor neurons, leading eventually to respiratory failure and death

252
Q

Is there a gender preference to ALS?

A

slightly more common in males

253
Q

Usual age of onset of ALS

A

50-60’s; early-onset cases have been seen

254
Q

Is there a genetic component to ALS?

A

most cases occur sporadically, but there are inherited forms: autosomal dominent, recessive, or X-linked

255
Q

What is the most common initial sx of ALS?

A

weakness or clumsiness, often focally then spreading to adjacent muscle groups

256
Q

Symptoms of ALS

A

Weakness or clumsiness, initially focally
painful muscle cramping and fasciculations
Bulbar complaints (dysarthria, dysphagia)
Respiratory comlaints

257
Q

What are neuro findings in ALS?

A 
Weakness
UMN and LMN findings (sometimes best in tongue)
Head droop
Pseudobulbar affect
Normal sensory and mental status exam
Extraocular muscles relatively spared
258
Q

What is seend on EMG of ALS patients?

A

evidence of muscle denervation and reinnervation in two or more extremities or body segments

259
Q

What is the life span of ALS patients?

A

23-52 months from onset

260
Q

What is the treatment for ALS and it’s mechanism of action

A

Rizuzole - blocks glutamate release; prolgons survival by several months

261
Q

What are important disorders to r/o in ALS?

A

lead toxicity, dysprteinemia, thyroid dysfunction, vitamin B12 deficiency, vasculitis, paraneoplastic syndromes, hexosaminidase A defciency, multifocal motor neuropathy with conduction block, cervical spine compression

262
Q

What is primary lateral sclerosis?

A

upper motor neuron disease

263
Q

Spinal muscular atrophy?

A

lower motor neuron disease

264
Q

Werdnig-Hoffmann disease?

A

spinal muscular atrophy occurrin gin in infancy, causes death by second year of life

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