Neuro 2 (Brainstem, PNS) Flashcards

1
Q

C1 dermatome

A

hairline

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2
Q

T4 dermatome

A

nipple line (male)

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3
Q

T10 dermatome

A

umbilicus

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4
Q

L1 dermatome

A

inguinal ligament

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5
Q

S1 dermatome

A

sole of foot

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6
Q

S4/5 dermatome

A

perianal

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7
Q

large cells/axons mediate

A

vibration and joint position sense

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8
Q

small cells/axons mediate

A

pain and temperature sensation

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9
Q

monomelic amyotrophy

A

Wasting in myotome
Self-limited
Electromyographic exam
May see MRI T2 signal

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10
Q

location of C6 root

A

between C5, C6

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11
Q

location of C8 root

A

between C7, T1

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12
Q

location of L4 root

A

between L4, L5

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13
Q

central protrusion in lumbar cord

A

affect descending root

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14
Q

lateral protrusion in lumbar cord

A

affects lateral roots

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15
Q

how to know it’s a radiculopathy?

A

Sensory and motor symptoms and signs in same dermatome and myotome

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16
Q

C5 radiculopathy = weakness in

A

Deltoid (C5, axillary)
Biceps (C5, musculocutaneous)
Infraspinatus (C5, suprascapular)
Rhomboid (C5, dorsal scapular)

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17
Q

Erb’s Palsy

A

upper plexus injury
Stretch upper roots (C5, C6)
Waiter’s tip
Musculocutaneous out

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18
Q

Klumpke’s Palsy

A

lower plexus traction injury
Pulling arm away from neck
Or nursemaid’s injury
Extensors out

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19
Q

How to know it’s a plexus injury

A

® Clinical-sensory, and motor deficits which do not fit a particular dermatoma/myotomal distribution or single nerve distribution
associated pain
usually unilateral

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20
Q

Parsonage Turner syndrome

A

□ Hereditary neuralgic amyotrophy
® Males»Females
® SEPT9 gene on chromosome 17w
® Septins are involved in formation of cytoskeleton
® Recurrent
Episide precipitated by physical activity

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21
Q

neuropraxia

A

temporary loss of motor and sensory function due to blockage of nerve conduction- focal demyelination

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22
Q

axonotmesis

A

disruption of axon w/ little disruption of CT

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23
Q

neurotmesis

A

disruption of axon and CT

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24
Q

Wallerian degeneration

A

degeneration of axon from distal to proximal. Associated w/ metabolic insufficiency

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25
Q

How to know it’s a mononeuropathy?

A

Sensory and motor symptoms and signs confined to distribution of one nerve

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26
Q

most common cause of polyneuropathy in US

A

diabetes

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27
Q

classification of polyneuropathy

A
vascular
infectious
neoplastic 
degenerative
inflammatory
congenital
autoimmune
trauma/toxins
endocrine
something else
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28
Q

how do we know it is a polyneuropathy?

A

Symptoms and signs in multiple nerves

Early neuropathy may not yet show motor or autonomic sxs

Symptoms and signs are length dependent, distal, symmetrical, dying back over time

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29
Q

Guillain-Barre syndrome (AIDP)

A

Bystander mechanism- antibody made against something else cross-reacts w/ myelin
Autoimmune process
Ascending weakness
Attacking the myelin- inflammatory mediators, damage the axon itself

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30
Q

Miller Fisher Variant

A

5% of GBC
Descending paralysis w/ triad: opthalmoplegia, ataxia (gait/trunk), areflexia
Anti GQ1B Ab in 85-90%
Tx: IVIg, PEx

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31
Q

Bickerstaff’s Encephalitis

A

Ataxia, cranial neuropathy, opthalmoplegia, altered mental status, hyperreflexia/Babinski
Anti-GQ1B Ab in 66%
Tx w/ steroids, IVIg, PEx

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32
Q

asymmetric polyneuropathy

A

demyelinating mononeuritis

multifocal motor neuropathy
small fiber neuropathy

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33
Q

Slow motor unit

A

Smaller forces
Maintain composure longer- resistant to fatigue due to subcellular anatomy
Important for posture, maintaining position

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34
Q

fast fatigable motor unit

A

Larger forces
Less myoglobin, fatigue easier
i.e. sympathetic response, standing jump (brief large forces)

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35
Q

fast fatigue resistant

A

Intermediate

Good for transition movements

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36
Q

2 ways to increase force (motor recruitment)

A

Enlist more friends –> increase number of motor units firing

Tell your friends to work harder –> increased firing frequency

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37
Q

Hallmarks of ALS Diagnosis

A

Combination of UMN and LMN signs
Can occur in 4 body regions: bulbar, cervical, thoracic, lumbosacral
Research requires 3/4 areas- may delay diagnosis and treatment
Rule out potentially treatable conditions mimicking this disorder

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38
Q

Upper motor neuron signs

A

Hyperreflexia
□ clonus
Spascicity
Upgoing toes (plantar extensor response)

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39
Q

Lower motor neuron signs

A

Weakness
Muscle atrophy
Fasciculations
Decreased/absent reflexes

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40
Q

Important negatives of ALS

A

Sensory systems in tact
Bowel/bladder dysfunction is spared
Ocular motor problems not effected

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41
Q

Poliomyelitis

A

□ Caused by RNA enterovirus
□ Eventually spreads to alpha motor neurons in spinal cord and brain stem
□ Causes focal atrophy and LMN findings

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42
Q

Spinal muscular atrophy

A

Bucket of autosomal recessive disorders
Survival motor neuron gene- important for alpha motor neuron to live
Looks like a LMN disease
Wernbig-Hoffman disease- huge spectrum of disease

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43
Q

muscular dystrophy

A

disease in muscle membrane or supporting proteins

ongoing muscle degeneration and regeneration

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44
Q

Duchenne/Becker MD

A
x-linked: mytation in dystrophin gene
important for structural integrity of muscles
Duchenne (absent), Beckers (low levels)
eventually lose walking ability
pseudohypertrophy
Gower's sign
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45
Q

Myotonic dystrophy Type 1

A

most common in adults

trinucleotide repeat disease in myotonin protein kinase

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46
Q

symptoms of myotonic dystrophy

A

ptosis, cataracts at early age (slit lamp needed)
Weakness- distal muscles get weak first
hypogonadism (reduced testosterone, testicular atrophy), reduced GH, insulin resistance, frequent loss of pregnancy
Afib, tachyarrhythmia, ectopic beats and cardiomyopathy late
dysphagia, hypokinetic tract w/ pseudo-obstruction, constipation

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47
Q

Fascioscapulohumeral MD

A

face, shoulder, arm
Reduction or deletion of DNA sequence- thought to be activator
70-90% AD inheritance
Highly penetrant- 90% of patients w/ weakness by age 20 w/ sizable deletion

CK values normal (creatine kinase- enzyme in muscles)

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48
Q

Fascioscapulohumeral MD Symptoms

A

Facial weakness early
Horizontal smile, wide palpebral fissures, difficulty burying eyelids and pursing lips
Weakness in arms –> medical attention –> anterior axillary folds
Scapular winging
Triple hump sign- fierce atrophy of deltoid, but trapezius and biceps are in tact
Abdominal laxity
Asymmetry- sometimes.

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49
Q

C fibers

A

nociception
slow conduction velocity
not tested by EMG

50
Q

When to order an EMG

A

Useful to exclude any peripheral cause of sensory or motor abnormalities on neurological exam when there is a diagnostic uncertainty

51
Q

what is on an NCS report

A

amplitude
conduction
latency
duration

52
Q

how to diagnose myopathy

A

EMG

sensory NCS is normal, as it conduction velocity and distal latency

53
Q

target fibers

A

seen in chronic denervation

54
Q

dysimmune/inflammatory myopathies

A

polymyositis
dermatomyositis
inclusion body myositis

55
Q

polymyositis

A

Cell mediated
Adults 40-70 yo
Proximal, symmetrical weakness and myalgia evolving (several months)
Lymphocytes (CD8+ T cells): w/in fascicules, surround, invade, and destroy myofibers

56
Q

dermatomyositis

A
Children and adults
Microvasculature
Association w/ malignancy
Proximal muscle weakness
Infiltrates B & CD 4+ T lymphocytes in interfascicular distribution
Heliotrope rash
57
Q

inclusion body myositis

A

mostly men
Pathology: inflammation, rimmed vacuoles
Congo red positive inclusions:
No effective treatment

58
Q

mitochondrial myopathies

A

ragged-red fiber

59
Q

GSE

A

somites- efferent

60
Q

GVE

A

sympathetic/parasympathetic

61
Q

SVE

A

branchial motor- derived from pharyngeal arch muscles

62
Q

GSA

A

sensation of external environment

63
Q

GVA

A

sensation of internal environment

carotid bodies, feedback system.

64
Q

SSA

A

vision
hearing
vestibular function

65
Q

SVA

A

chemical transmission:

olfaction, taste

66
Q

lesion on XII in cortex

A

contralateral tongue deviation

67
Q

lesion on XII nucleus, fascicles, or nerve

A

ipslateral tongue deviation

68
Q

lesion on XI in R cortex

A

L trapezius, R SCM weakness

head deviates toward the R

69
Q

lesion on R XI nerve itself

A

R trapezius, R SCM weakness

if anything, deviation toward R

70
Q

vagus nerve nuclei

A

Dorsal motor nucleus
Nucleus ambiguus
Solitary tract/nucleus
Spinal trigeminal nucleus

71
Q

Dorsal motor nucleus

A

parasympathetic

72
Q

Nucleus ambiguus

A

branchial motor supply (arch 4-6)

73
Q

Solitary nucleus

A

visceral sensation, taste

74
Q

Uvular deviation

A

deviates towards the good side (away from the lesion)

Dysphagia: cortical lesion
Focal swallowing dysfunction/hoarseness: nerve lesion

75
Q

rostral part of nucleus solitarius

A

gustatory nucleus- taste

76
Q

caudal part of nucleus solitarius

A

cardiorespiratory nucleus- chemo and baroreceptors

from aortic arch, cardiorespiratory system, digestive tract

77
Q

big difference between IX and X

A

parasympathetics:
IX: from inferior salivatory nucleus to parotid gland. Sympathetics synapse in otic ganglion

78
Q

area postrema

A

open BBB

center for vomiting, closely related to CN X

79
Q

CN VIII- type of fibers

A

all SSA

80
Q

pathway of sound

A
cochlear nuclei
decussation in trapezoid body
superior olivary nucleus
lateral lemniscus
inferior colliculus
medial geniculate body of thalamus
auditory cortex- frontal lobe
81
Q

nuclei of facial nerve

A

spinal trigeminal
solitary nucleus
superior salivatory nucleus

82
Q

VII: branchial motor

A

facial motor nucleus and nerve fascicle

to muscles of facial expression, posterior belly of digastric, stylohyoid, stapedius

83
Q

upper face innervation

A

ipslateral and contralateral contribution

84
Q

lower face innervation

A

only contralateral side

85
Q

VII lesion in UMN

A

contralateral weakness of lower face only

86
Q

VII lesion in LMN

A

all fibers to one side of face (upper and lower face)

87
Q

VII parasympathetics

A

from superior salivatory nucleus
via greater petrosal nerve
synapse in sphenopalatine ganglion
all salivary glands except for parotid

88
Q

IX parasympathetics

A

inferior salivatory nucleus

89
Q

VII taste

A

nucleus solitarius (rostral)–> geniculate ganglion–> central tegmental tract –> thalamus –> insularr cortex –>…

90
Q

VII GSA

A

cell bodies in geniculate ganglion

91
Q

exit of CN VI

A

superior orbital fissure

92
Q

does V have parasympathetics?

A

no, just motor and sensory

93
Q

location of VI, 2, 3 cell bodies

A

trigeminal ganglion

94
Q

V1 exit

A

superior orbital fissure

95
Q

V2 exit

A

foramen rotundum

96
Q

V3 exit

A

foramen ovale

does NOT pass through cavernous sinus

97
Q

what is alone in the cavernous sinus?

A

VI

98
Q

SVE of VII

A

to muscles of mastication, a nterior belly of digastric, tensor tympani, tensor velli palatini

99
Q

lesion in V3

A

jaw deviation toward the weak side (due to pterygoids)

100
Q

V for proprioception

A

GVA for fine touch- mesencephalic nucleus and tract

101
Q

where is the cell body for V proprioceptive neurons?

A

mesencephalic nucleus

102
Q

corneal reflex

A

in on V –> blinking VII

103
Q

types of fibers in IV

A

GSE

104
Q

parasympathetic nucleus for III

A

edinger-westphall

105
Q

DRG history

A

Pain and numbness in dermatomal distribution
Decreased sensation in dermatomal distribution
Trouble with balance/coordination
No weakness- no motor

106
Q

APD

A

○ Damage to the optic nerve or bad retinal disease
○ Not seen with cataracts, vitreous or corneal disease, refractive error
○ Not seen in functional (non-organic disease)

107
Q

cocaine test

A

blocks reuptake of NE. Dilation is normal.

with Horner’s syndrome, nothing happens.

108
Q

apraclonidine

A

alpha adrenergic agonist
reversal of Horner’s syndrome
denervation supersensitivity

109
Q

Adie’s Pupil

A

Occurs in young woman, benign, probably viral
Unlike pharm blockage, you constrict to near
Also reacts to dilute pilocarpine (1/8%) unlike the normal pupil
no response to light, but response to near
absent reflexes

110
Q

binocular vision

A

sign of issue on efferent side, likely ocular misalignment

111
Q

worse diplopia at a distance

A

VI

112
Q

worse diplopia near

A

III, medial rectus

113
Q

vertical diplopia

A

III, IV
myasthenia gravis
thyroid eye disease

114
Q

benign positional vertigo

A

last less than a minute- positional

115
Q

Meniere’s disease

A

lasts hours usually with tinnitus (ringing noise) and hearing loss

116
Q

Vestibular neuritis

A

inflammation of the inner ear- last days to weeks

117
Q

Acoustic neuroma

A

evolves over weeks to months

118
Q

pathologic nystagmus characteristics

A

amplitude greater than 4 degrees
asymmetry
commonly caused by drugs and anti-seizure meds
doesn’t fatigue with prolonged gaze

119
Q

peripheral nystagmus

A

beats in one direction regardless of gaze

120
Q

central nystagmus

A

vertical component, direction changing