Ch. 6 One-liners Flashcards
1
Q
Function of the lateral cortico-spinal tract
A
Motor
2
Q
Function of the posterior columns
A
Sensory (vibration, propriosension, fine touch)
3
Q
Function of anterolateral pathway
A
Sensory (pain, temperature, crude touch)
4
Q
Sulcus that divides the frontal obe from the parietal lobe
A
Central/Rolandic sulcus
5
Q
Location of primary motor cortex
A
precentral gyrus (Brodmann’s 4)
6
Q
Location of primary somatosensory cortex
A
postcentral gyrus (Brodmann’s 3, 1, 2)
7
Q
brodmann’s area for primary motor cortex
A
four
8
Q
brodmann’s areas for primary somatosensory cortex
A
3, 1, and 2
9
Q
Lesions in the primary motor and primary somatosensory cortex cause what deficits?
A
motor or sensory deficits, respectively, in the contralateral body
10
Q
Location of premotor cortex
A
just anterior to the primary motor cortex (Brodmann’s 6); (laterally)
11
Q
Location of the suuplementary motor area
A
just anterior to the primary motor cortex (Brodmann’s 6) (medially)
12
Q
Function of premotor cortex and supplementary motor areas
A
higher-order motor planning
13
Q
Location of parietal association cortex
A
parietal lobe posterior to primary somatosensory cortex, superior parietal lobule (Brodmann’s 5, 7)
14
Q
Location of Secondary somatosensory area
A
Parietal operculum (posterior to primary somatosensory cortex, laterally)
15
Q
Function of somatoesosory association cortex
A
higher-order sonsory processing
16
Q
Lesions in the sensory or motor association cortex cause what deficits?
A
higher-order sensory analysis or motor planning
17
Q
How is the cortex organized?
A
somatotopically, depicted by the humunculus
18
Q
What is the somatotopic respresentation?
A
arms medial to legs with two exceptions: primary sensorimotor cortices and posterior columns
19
Q
Where are sensory neurons located?
A
dorsal root ganglia
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
21
Q
What is the dorsal horn for?
A
sensory processing
22
Q
What is the ventral horn for?
A
contains motor neurons
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
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
25
What is contained within the intermediate zone?
interneurons and certain specialized nuclei
26
What are the nuclei of the intermediate zone?
Clarke's nucleus, intermediolateral nucleus
27
What are the nuclei of the ventral horn?
Medial motor nucleus
Commissural nucleus
Lateral motor nucleus
28
What is the nuclei in the gray matter surrounding the central canal?
Grisea centralis
29
What Bror Rexed Laminae is represented by the marginal zone?
I
30
What Bror Rexed Laminae is represented by the substantia gelatinosa?
II
31
What Bror Rexed Laminae is represented by the nucleus proprius?
III and IV
32
What Bror Rexed Laminae is represented by the neck of the dorsal horn
V
33
What Bror Rexed Laminae is represented by the base of the dorsal horn?
VI
34
What Bror Rexed Laminae is represented by The intermediate zone (Clarke's nucleus and intermediolateral nucleus?
VII
35
What Bror Rexed Laminae is represented by the commissural nucleus
VIII
36
What Bror Rexed Laminae is represented by The medial and lateral motor nuclei?
IX
37
What Bror Rexed Laminae is represented by the grisea centralis?
X
38
columns of white matter in spinal cord
dorsal (posterior), lateral, and ventral (anterior) columns
39
where is white matter the thickest in the spinal cord
cervical levels where most ascending fibers have entered and more descending fibers have not terminated
40
where is there more gray matter in the spinal cord
cerival and lumbosacral, esp. in ventral horn due to nerve plexuses for arms and legs
41
where is the intermediolateral cell column
lateral horn in thoracic cord
42
What characterizes the sacral cord?
mostly gray matter
43
What characterizes the cervical cord?
white matter is the thickest
44
What characterizes the thoracic cord?
lateral horn containing intermediolateral cell column
45
What is the cervical enlargement?
gives rise to the nerve plexus for the arms
46
What is the lumbosacral enlargement?
gives rise to the nerve plexus for the legs
47
Spinal levels of cervical enlargement
C1-T3
48
Spinal levels of lumbosacral enlargement?
L1-S2
49
What is the blood supply to the spinal cord?
anterior and posterior spinal arteries forming the spinal arterial plexus, and radicular arteries
50
What gives rise to the anterior spinal artery?
Vertebral arteries
51
What does the anterior spinal artery supply?
anterior 2/3rds of cord (anterior horns and anterior and lateral white matter columns)
52
What gives rise to the posterior spinal artery?
posterior inferior cerebellar artery (PICA) and vertebral arteries
53
What does the posterior spinal artery supply?
posterior 1/3 of the cord (posterior columns and part of posterior horns)
54
Describe the involvement of the aorta in blood supply to the cord?
gives rise to 31 segmental branches that enter the spinal canal; most supply the meninges; 6-10 reach the spinal cord as radicular arteries
55
What gives rise to radicular arteries and how many are there?
aorta, 6-10
56
What is the great radicular artery of Adamkiewicz?
a prominent radicular artery that is major blood supply to the lumbar and sacral cord
57
Spinal level of great radicular artery of Adamkiewicz?
usually b/w T9-T12; but can be anywhere b/w T5-L3
58
What is the vulnerable zone of the cord?
an area of relatively decreased perfusion between the lumbar and vertebral arterial supplies; located in mid-thoracic region at about T4-T8
59
Where is the vulnerable zone located?
mid-thoracic; T4-T8
60
What is the significance of the vulnerable zone?
susceptible to infarct during thoracic surgery or conditions that cause decreased aortic pressure
61
What is the venous drainage of the spinal cord?
Batson's plexus - a plexus of veins in the epidural space
62
Explain how metastatic cells from prostate cancer or a pelvic infection might enter the epidural space?
the epidural veins of Batson's plexus don't contain valves, allowing reflux of blood with increased intra-abdominal pressure
63
What is apraxia? Lesions where may cause it?
deficit in higher-order motor planning and execution despite normal strength;
caused by lesions in association areas
64
Where are upper motor neurons located?
cerebral cortex
65
Where are lower motor neurons located?
spinal cord and brainstem
66
Where are lateral motor systems located in the spinal cord?
travel in lateral columns, synapse on lateral ventral horn motor neurons and interneurons
67
Where are medial motor systems located in the spinal cord?
travel in anteromedial spinal cord, synapse on the medial ventral horn motor neurons or interneurons
68
What tracts carry the lateral motor systems?
lateral corticospinal tract and rubrospinal tract
69
Function of lateral corticospinal tract
movement of contralateral limbs (esp. rapid, dextrous movements of individual digits or joints)
70
What is the site of origin of the lateral corticospinal tract?
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)
71
Where does the lateral corticospinal tract decussate?
pyramidal decussation, at the cervicomedullary junction
72
Termination of lateral corticospinal tract
Entire cord (predominantly at cervical and lumbosacral enlargements)
73
What is the most clinically important motor tract?
lateral corticospinal tract
74
Function of rubrospinal tract
movement of contralateral limbs
taking over after cotricospinal injury
flexor posturing of upper extremity
seen in lesions above red nuclei when it is spared
75
Origin of rubrospinal tract
Red nucleus, magnocellular division
76
Termination of rubrospinal tract
cervical cord
77
Decussation of rubrospinal tract
ventral tegmental decussation, in midbrain
78
What tracts are involved with the medial motor system?
anterior corticospinal tract
medial and lateral vestibulospinal tracts
reticulospinal tracts
tectospinal tracts
79
Function of anterior corticospinal tract
contraol of bilateral axial and girdle muscles (postural tone and balance)
80
Function of medial VST
positioning of head and neck
81
Function of lateral VST
balance
82
Termination level of medial VST
cervical and upper thoracic cord
83
Termination level of lateral VST
entire cord
84
Origin of anterior corticospinal tract
primary motor cortex and supplementary motor area
85
Origin of medial VST
medial and inferior vestibular nuclei
86
Origin of lateral VST
lateral vestibular nucleus
87
Function of reticulospinal tracts
automatic posture and gait-related movements
88
Origine of reticulospinal tracts
pontine and medullary reticular formation
89
Termination level of reticulospinal tracts
entire cord
90
Function of tectospinal tract
coordination of head and eye movement
91
Origin of tectospinal tract
superior colliculus
92
Decussation of tectospinal tract
dorsal tegmental decussation, in midbrain
93
Decussation of anterior corticospinal tract
n/a
94
Decussation of vestibulospinal tracts
n/a
95
Decussation of reticulospinal tracts
n/a
96
Explain why a unilateral lesion to the medial motor system causes no obvious deficits?
they terminate on interneurons that project to both sides of the psinal cord, controlling mevements that involve bilateral spinal segments
97
Cortical layer of the lateral croticospinal tract
5
98
Where do layer 5 pyramidal cells synapse
directly onto motor neurons in the ventral horn, and spinal interneurons
99
What are Betz cells
the largest neurons in the nervous system, comprise 3% of corticospinal neurons
100
Where do axons from cerebral cortex of lateral corticospinal tract go
upper portion of cerebral white matter (corona radiata), descend toward internal capsule
101
What does cerebral white matter convey
bidirection info btwn different cortical areas, btwn cortex and deep structures (like basal ganglia, thalamus, and brainstem)
102
location of internal capsule
thalmus and caudate nucleus are always medial to and globus pallidus and putamen are always lateral to
103
three parts of internal capsule
anterior limb, posterior limb, genu
104
anterior limb separates
separates head of caudate from the globus pallidus and putamen
105
posterior limb separates
separates thalamus from globus pallidus and putamen
106
genu location
transition from anterior and posterior limbs at the level of the foramen of Monro
107
where is the corticospinal tract in the internal capsule
posterior limb
108
corticobulbar fibers
project from cortex to brainstem (bulb); contain motor fibers for the face
109
orientation of somatotopic map in corticospinal tract
anterior to posterior and medial to lateral: face, arm, trunk, leg
110
What is the effect of a lesion of the lateral corticospinal tract at the level of the internal capsule
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
what does the internal capsule continue into
midbrain cerebral peduncles
112
What are the parts of the cerebral peduncle
substantia nigra and basis pedunculi
113
Where is the white matter contained in the cerebral peduncle
basis pedunculi (ventral portion)
114
Where are the corticobulbar and corticospinal tracts located in the midbrain?
the middle third of the basis pedunculi
115
What is the somatotopic organization of the corticospinal fibers in the basis pedunculi?
medial to lateral: face, arm, trunk, leg
116
What is contained in other portions of the basis pedunculi?
primarily corticopontine fibers
117
Describe the path of the corticospinal fibers:
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
where do corticospinal fibers travel after basis pedunculi
descend through ventral pons forming scattered fascicles on the basis pontis
119
where do the scattered fascicles of the corticospinal tract collect
ventral/rostral surface of medulla to form medullary pyramids
120
What is the cervicomedullary junction?
transition from medulla to spinal cord
121
What is the level of the cervicomedullary junction?
foramen magnum
122
What occurs to corticospinal tract at cervicomedullary jxn
85% pyramidal tract fibers cross over in pyramidal decussation to enter lateral white matter columns - forming the lateral corticospinal tract
123
What occurs to remaining 15% of corticospinal fibers
continue ipsilaterally without crossing and enter anterior white matter columns
124
What is another name for the corticospinal tract?
pyramidal tract (because fibers collect on the medullary pyramids)
125
What is the somatotopic organization of the lateral corticospinal tract?
medial to lateral: arms, trunk, leg
126
Where is the lateral corticospinal tract located in the spinal cord?
lateral columns
127
Where do lateral corticospinal tract fibers synapse?
anterior horn cells (gray matter)
128
How do autonomic efferents differ anatomically from somatic efferents?
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
What is the enteric nervous system
a third autonomic division consisting of a nerual pleuxus w/in the walls of the gut; controls peristalsis and GI secretions
130
where are preganglionic neurons of the sympathetic division located
intermediolateral cell column, in lamina VII (intermediolateral nucleus) of spinal cord levels T1 to L2?3
131
what are the two sets of sympathetic ganglia
paired paravertebral sympathetic trunk ganglia (aka sympathetic chain) and unpaired prevertebral ganglia
132
What are the sympathetic chain ganglia from T1-T3?
superior, middle (often absent), and iferior/stellate cervical ganglia
133
Where are the prevertebral ganglia located?
in the celiac plexus surrounding the aorta
134
What are the prevertebral ganlgia?
celiac, superior mesenteric, and inferior mesenteric ganlgia
135
where do parasympathetic preganglionic fibers arise from?
cranial nerve parasympathetic nuclei and sacral parasympathetic nuclei
136
Where are the sacral parasympathetic nuclei located?
lateral gray matter of S2-S4, in a location similar to the intermediolateral cell column
137
What do sympathetic postganglionic fibers release?
norepinephrine; EXCEPTION: sweat glands are Ach
138
What do parasympathetic postganglionic fibers release?
acetylcholine
139
What do preganglionic fibers release?
acetylcholine
140
What is a treatment for hyperhidrosis and describe the mechanism
botulinum toxin - blocks cholinergic receptors, so is injected locally into the skin of the axilla
141
What are signs of LMN injury?
```
muscle weakness
atrophy
fasciculations
decreased tone
hyporeflexia
```
142
What are signs of UMN?
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
What are fasciculations?
abnormal muscle twitches caused by spontaneous activity in groups of muscle cells
144
What is spasticity?
increased tone and hyperreflexia
145
What is flaccid paralysis?
decreased tone and reflexes seen in acute UMN injuries
146
What is an example of an UMN injury causing flaccid paralysis?
spinal shock
147
what receptors do parasympathetic postganglionic neurons activate
muscarinic cholinergic receptors (M1-3)
148
what receptors do preganglionic neurons activate
nicotinic receptors (acetylcholine)
149
what are sympathetic and parasympathetic outflow controlled by
directly and indirectly by higher centers like hypothalamus, brainstem nuclei (nucleus soltaris), amygdala, several regions of limbic cortex
150
what else can autonomic responses be regulated by
afferent sensory info (chemoreceptors, osmoreceptors, thermoreceptors, baroreceptors)
151
receptors of postganglionic sympathetic neurons
alpha 1, alpha 2, beta 1, beta 2, beta 3
152
acute UMN lesion
initially flaccid paralysis with decreased tone and reflexes, which gradually change over hours/months into spastic paresis
153
hypothesized mechanism of spasticity
caused by damage to descending inhibitory pathways that travel closely with the corticospinal tract, not damage to the spinal tract itself
154
What is Hoffmann's sign?
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
What would you name unilateral face, arm, and leg weakness or paralysis?
Hemiparesis or hemiplegia; or pure motor hemiparesis
156
Why is the spinal cord ruled out in pure motor hemiparesis?
becase the face would be spared with spinal cord lesions
157
Why is pure motor hemiparesis? unlikely to be cortical?
the lesion would have to involved the entire strip, in which case sensory involvement in hard to avoid
158
Why is hemiparesis/hemiglegia unlikely to be muscle or peripheral nerve?
coincidental involvement of the face, arm and leg, all on one side of the body is unlikely
159
Location of lesion in pure motor hemiparesis
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
What is the side of the lesion in hemiparesis/hemiplegia/pure motor hemiparesis?
contralateral (above the pyramidal decussation)
161
What are common causes of pure motor hemiparesis?
lacunar infarct of internal capsule or pons, less commonly infarct of cerebral peduncle; demyelination, tumor, or abscess in these location or corona radiata
162
What arteries would be involved with lacunar infarct of the internal capsule?
lenticulostriate branches of the middle cerebral artery or anterior choriodal artery
163
What arteries would be involved with lacunar infarct of the pons?
median perforating branches of the basilar artery
164
What are associated features of hemiparesis/hemiplegia/pure motor hemiparesis?
UMN signs usually present
dysarthria-pure motor hemiparesis
ataxia-hemiparesis
165
What causes ataxia in ataxia-hemiparesis?
involvement of the cerebellar pathways (corticopontine fibers)
166
Location of lesion in hemiparesis/hemiplegia associated with somatosensory, oculomotor, viusal, or higher cortical deficits (like aphasia or neglect)
Entire primary motor cortex (precentral gyrus), or corticospinal and corticobulbar tract fibers above the medulla
167
Assocaited features of hemiparesis with associated somatosensory, oculomotor, visual, or higher cortical deficits
UMN signs usually present
dysarthria possibly
ataxia possibly
168
What is brachiocrural plegia/paresis?
hemiplegia/hemiparesis sparing the face; i.e. unilateral arm and leg weakness/paralysis
169
Why wouldn't brachiocrural plegia/pareses lesions be in the corticospinal tract below the motor cortex above the medulla?
The corticobulbar tract is located very close - thus the face would likely be involved
170
Why wouldn't brachiocrural plegia/paresis be muscle or peripheral nerve lesions?
It is unlikely to be coincidental involvement of both the arm and leg on one side of the body
171
Why wouldn't brachiocrural plegia/paresis lesions be below C5?
In that case, some arm muscles would be spared.
172
What are the most likely locations of lesions for brachiocrural plegia/paresis and what side in relation to weakness?
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
Associated features allowing further localization for hemiparesis sparing the face
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
Common causes of hemiparesis sparing the face:
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
What is faciobrachial paresis/plegia?
unilateral face and arm wekaness/paralysis
176
Why is a lesion in the internal capsule or below unlikely (but not impossible) in faciobrachial paresis?
the corticobulbar and corticospinal tracts are failry compact, resulting in leg involvement
177
Location of lesions involved in faciobrachial paresis/plegia
face and arm areas of the primary motor cortex, over the lateral frontal convexity; contralateral
178
Associated features allowing further localization for faciobrachial paresis/plegia
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
What is the classic cause of faciobrachial paresis/plegia?
middle cerebral artery superior division infarct
180
What is another name for unilateral arm weakness or paralysis?
brachial monoparesis/monoplegia
181
What is a rare cause of unilateral arm weakness/paralysis?
foramen magnum tumors may initially affect one arm
182
Location of lesion in unilateral arm weakness/paralysis
contralateral arm area of the primary motor cortex; ipsilateral peripheral nerves supplying the arm
183
Associated features allowing further localization of unilateral arm weakness/paralysis
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
Common causes of unilateral arm weakness/paralysis:
motor cortex: infarct of small cortical branch of middle cerebral artery, or small tumor or abscess
peripheral lesion: compression injury, diabetic neuropathy, etc.
185
Crural monoparesis/monoplegia
unilateral leg weakness or paralysis
186
Location involved with crural monoparesis/plegia
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
Associated features allowing localization of crural monoparesis/plegia
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
Causes of crural monoparesis/plegia:
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
Names for unilateral facial weakness/paralysis:
Bell's palsy (peripheral nerve); isolated facial weakness
190
What locations are r/o in unilateral facial weakness/paralysis
below the rostral medulla
191
Locations involved in unilateral facial weakness or paralysis:
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
Associated features of unilateral facial weakness/paralysis:
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
What is facial diplegia?
bilateral facial weakness; difficult to detect
caused by: motor neuron disease, bilateral peripheral nerve lesions, bilateral white matter abnormalities (ischemia or demyelination)
194
Brachial diplegia
bilateral arm weakness
195
Locations involved in brachial diplegia
Medial fibers of both lateral corticospinal tracts
B/l cervical spine ventral horns
Peripheral nerve or muscle disorders affecting both arms
196
Associated features in brachial diplegia
central or anterior cord syndromes can help localize
197
Common causes of brachial diplegia
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
Paraparesis/plegia
bilateral leg weakness/paralysis
199
Locations of paraperesis/plegia
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
Associated localizing features of paraperesis/plegia:
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
Causes of paraperesis/plegia
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
Names for bilateral arm and leg weakness or paralysis
Quadriparesis, quadriplegia, tetraparesis, tetraplegia
203
Why is the motor cortex below the motor cortex and above the medulla r/o in bilateral arm and leg weakness?
face would be involved
204
Why is spinal cord below C5 unlikely in bilateral arm and leg weakness/paralysis?
arms would be partly spared
205
Locations involved in bilateral arm and leg weakness/paralysis
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
Associated localizing features of quadraparesis/plegia
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
Common causes of bilateral arm and leg weakness/paralysis
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
Locations r/o in generalized weakness or paralysis
small focal or unilateral lesions
| lesions of lower medulla or spinal cord (spare face or UE)
209
Locations involved in generalized weakness or paralysis
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
Associated features allowing localization of generalized weakness
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
Common causes of generalized weakness or paralysis
global cerebral anoxia, pontine infarct or hemorrhage (locked-in), amyotrophic lateral sclerosis, Guillain-Barre, myasthenia, botulism, numerous other
212
Spastic gait
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
Localization of spastic gain
corticospinal tracts (unilateral or bilateral)
214
Ataxic gait
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
Localization of ataxic gait
cerebellar vermis or other midline cerebllar structures
216
Vertiginous gait
looks similar to ataxic gait: wide based and unsteady. Positive Romberg sign
217
Localization of vertiginous gait
vestibular nuclei, vestibular nerve, semicircular canals
218
Frontal gait
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
Localization of frontal gait
frontal lobes or frontal subcortical white matter
220
Parkinsonian gait
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
Localization of Parkinsonian gait
sustantia nigra or other regions of the basal ganglia
222
See table 6.6
pg. 251-252 for gait causes
223
Dyskinetic gait
dancelike (choreic), glinging (ballistic), or writhing (athetoid) movements with walking, may be accompanied by some unsteadiness
224
Localization of dyskinetic gait
subthalamic nucleus, other regions of the basal ganglia
225
Tabetic gait
high-stepping, foot flaaping, with particular difficulty walking in the dark or on uneven surfaces; Romberg sign present
226
Localization of Tabetic gait
posterior columns or sensory nerve fibers
227
Paretic gait
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
Localization of paretic gait
nerve roots, peripheral nerves, neuromuscular jxn, or muscles
229
Antalgic gait
painful; pain may be obvious based on report of facial expression; avoids putting pressure on affected limb
230
Localization of antalgic/painful gait
peripheral nerve or orthopedic injury
231
Orthopedic gait disorder
depends on nature and location; peripheral nerve injury or spinal cord-related deficits may also be present
232
Localization of orthopedic gait disorder
bones, ligaments, tendons, joints, muscles
233
Functional gait disorder
hard to dx; reports of poor balance yet sponatneously perfrom highly destabilizing swaying movements while walking, without ever falling
234
Localization of functional gait disorder
psycholigically based
235
What is multiple sclerosis?
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
Why do some patients with MS have worse sx when they are warm?
dispersion of action potentials increases with temperature
237
What is the classic clinical definition of MS?
Two or more deficits separated in neuroantatomical space and time
238
What are MRI findings of MS?
oligoclonal bands, white matter lesions/plaques, T2-bright areas, Dawson's fingers, acute plaques enhances with gadolinium
239
What are oligoclonal bands?
discrete bands on gel electrophoresis resulting from synthesis of large amounts of immnoglobulin by individul plasma cell clones in the CSF
240
What are unusual CSF findings in MS patients? (help r/o MS)
>50 WBCs or with CSF with nonlymphocytes
241
What do T2-bright areas represent in MS patients on MRI?
demyelinative plaques in white matter
242
Where are T2-bright areas located in MRI of MS patients?
extending into white matter from periventricular locations - resulting in Dawson's fingers; located in supratentorial and infratentorial structures
243
What are Dawson's fingers?
MS plaques extending into the twhite matter from periventricular locations
244
What can enhance acute plaques in the MRI of MS patients?
Gadolinium
245
50% of patients with what sx develop MS?
single episode of optic neuritis or transverse myelitits
246
What is the course of MS?
relapsing-remitting, but evolves into a more refractory chronic progressive
247
What is the therapy for acute exacerbation of MS?
high-dose steroids (speeds recovery but doesn't effect overall course)
248
What is the first-line therapy for relapsing-remitting MS?
beta-IFN and copolymer (glatiramer acetate) - prevent exacerbations and delay progression
249
What are second line treatments for MS?
monoclonal antibodies - natalizumab, rituximab, campath
| chemotherapeutic agents: cyclophosphamide, mitoxantrone
250
What are motor neuron diseases?
disorders, mostly degenerative, that selectively affect UMNs, LMNs or both, producing motor deficits without sensory abnormalities or other findings
251
What is ALS?
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
Is there a gender preference to ALS?
slightly more common in males
253
Usual age of onset of ALS
50-60's; early-onset cases have been seen
254
Is there a genetic component to ALS?
most cases occur sporadically, but there are inherited forms: autosomal dominent, recessive, or X-linked
255
What is the most common initial sx of ALS?
weakness or clumsiness, often focally then spreading to adjacent muscle groups
256
Symptoms of ALS
Weakness or clumsiness, initially focally
painful muscle cramping and fasciculations
Bulbar complaints (dysarthria, dysphagia)
Respiratory comlaints
257
What are neuro findings in ALS?
```
Weakness
UMN and LMN findings (sometimes best in tongue)
Head droop
Pseudobulbar affect
Normal sensory and mental status exam
Extraocular muscles relatively spared
```
258
What is seend on EMG of ALS patients?
evidence of muscle denervation and reinnervation in two or more extremities or body segments
259
What is the life span of ALS patients?
23-52 months from onset
260
What is the treatment for ALS and it's mechanism of action
Rizuzole - blocks glutamate release; prolgons survival by several months
261
What are important disorders to r/o in ALS?
lead toxicity, dysprteinemia, thyroid dysfunction, vitamin B12 deficiency, vasculitis, paraneoplastic syndromes, hexosaminidase A defciency, multifocal motor neuropathy with conduction block, cervical spine compression
262
What is primary lateral sclerosis?
upper motor neuron disease
263
Spinal muscular atrophy?
lower motor neuron disease
264
Werdnig-Hoffmann disease?
spinal muscular atrophy occurrin gin in infancy, causes death by second year of life
