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Eugenie Notes > Notes 3A > Flashcards

Notes 3A Flashcards

1
Q

F wave?

A

obtained after super maximal stimulation of a motor nerve
electrical impulse travels antidromically (conduction along the axon opposite to the normal direction of the impulses) along the motor axons toward the motor neuron, backfiring and then orthodromically (conduction along the motor axon in the normal direction) down the nerve to be recorded at the muscle.

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2
Q

H reflex?

A

electrophysiologic equivalent of the ankle reflex (S1 reflex arc) and is obtained by stimulating the tibial nerve at the popliteal fossa while recording at the soleus.

The electrical impulse travels orthodromically through a sensory afferent, enters the spinal cord, and synapses with the anterior horn cell, traveling down the motor nerve to be recorded at the muscle

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3
Q

Siponimod? MOA and SE?

A

sphingosine 1 -P inhibitor
Need to check CYP2A9 prior to initiating treatment

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4
Q

Ocrelizumab MOA? only DMT approved for?

A

Anti-CD20
Only one approved for PPMS

*can have infusion reactions, tx with tylenol and solumedrol*

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5
Q

Large polyphasic motor unit potentials are seen in?

A

chronic re-innervation

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6
Q

Types of spontaneous activity?

A

fibrillation potentials
fasciculation potentials
myokymia
myotonic potentials

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7
Q

What is recruitment?

A

measure of the number of MUPs firing during inc force of voluntary muscle contractionm

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8
Q

myopathic MUAPs are

A

small and short in duration

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9
Q

neurogenic MUAPs are

A

large and prolonged

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10
Q

Fibrillation potentials

A

occur when an individual muscle is denervated. Fibrillation potentials are small (<500 µV), short (<5 ms in duration), biphasic or triphasic, and fire regularly or sometimes irregularly.

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11
Q

Positive sharp waves

A

emanate from denervated muscle fibers and have the same clinical significance as fibrillations. They have a sharp initial positive deflection followed by a longer, lower amplitude negative phase than fibrillation potentials.

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12
Q

Myokymia

A

Myokymia consists of bursts of MUAPs, usually 2 to 10, firing at rates of 20 to 150 Hz. The bursts consist of regular or irregular doublets, triplets, or multiplets. Between bursts there is electrical silence.

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13
Q

Reduced recruitment is when there is? seen in

A

less than expected MUPs firing more rapidly than expected

axonal loss, conduction block, end stage myopathy

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14
Q

Early or rapid recruitment is when there is?

A

myopathic processes with lots of muscle fibers in which an excessive number of short-duration and small amplitude MUPs fire during contraction

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15
Q

With poor effort or with CNS disorders causing weakness, recruitment is?

A

reduced, with normal MUPs firing at slow or moderate rates

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16
Q

In neuropathic disorders with denervation and re-innervation, MUPs are

A

inc duration and amplitude, and may be polyphasic

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17
Q

In a radiculopathy, SNAPs are

A

normal (SNAPs are recorded distally to the lesion, in the postganglionic projections from the DRG)

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18
Q

EMG findings in radiculopathy?

A

An axon loss radiculopathy will also injure motor fibers in the intraspinal canal region affecting the respective myotome.

This leads to denervation, with fibrillation potentials seen 3 weeks after the onset of motor axon loss, decreased recruitment, and 3 to 6 months later, large and polyphasic motor unit potentials (MUPs). The presence of these large and polyphasic MUPs is dependent on reinnervation and collateral innervation, typically occurring in a proximal to distal fashion, with proximal muscles more successfully reinnervated as compared to distal muscles.

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19
Q

Mg dx with EMG/NCS

A

NCS is normal EMG with slow repetitive nerve stimulation showing more than 10% decremental response in CMAP amplitude

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20
Q

Lambert Eaton Dx with EMG/NCS

A

rapid stimulation produces an incremental increase in CMAP amplitude (>50% inc)

  • this occurs with rapid stimulation (20 to 50 Hz) because the frequency of stimulation is faster than the time it takes for calcium to leave the presynaptic terminal (100 to 200 ms), leading to higher levels of calcium influx and larger end-plate potentials
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21
Q

Skeletal muscle Type 1

A

slow-oxidative

  • slow ATPase activity and large oxidative capacity
  • Large num of mitochondria
  • Red in color, small diameter
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22
Q

Skeletal muscle type 2A

A

fast oxidative glycolytic fibers

  • Fast ATPase
  • High glycolytic capacity
  • Moderate oxidative capacity
  • Fast and resistant to fatigue
  • Red and large
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23
Q

Skeletal muscle type 2B

A

fast oxidative glycolytic fibers

  • Fast ATPase
  • High glycolytic capacity
  • Low oxidative capacity
  • Fast and fatigable
  • Pale and large
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24
Q

CIDP

features

timeline

EMG/NCS shows

Biopsy?

A

symmetric demyelination with proximal and distal weakness with or without sensory loss and hypo/areflexia.

progressive, needs to be for 8 weeks for dx

demyelinating polyneuropathy with prolongation of distal motor latencies, reduction of motor conduction velocities, prolongation of F-wave latencies/absence of F-wave, partial motor conduction block, abnormal temporal dispersion

onion-bulb formation

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25
Q

normal latency should be? conduction velocity?

A

<4 ms

>50

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26
Q

The presence of a conduction block suggests?

A

demyelination

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27
Q

Wallerian degeneration is completed in ___ days from the injury

A

7-10

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28
Q

Fibrillation potentials (sign of spontaneous muscle activity) appear in ___ days from injury

A

3 weeks( 21 days)

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29
Q

Carpal tunnel

where is sensation spared?

A

thenar eminence because the palmar sensory branch that innervates the thenar eminence travels outside the carpal tunnel

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30
Q

Sign of severe CTS is

A

thenar muscle atrophy

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31
Q

GBS: which variant has worse prog

A

axonal variant

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32
Q

NIF of less than ___ or vital capacity less than ___ supports elective intubation in GBS

A

-30

15-20

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33
Q

Which nerves branch off the roots of the brachial plexus

A

dorsal scapular nerve (innervates the rhomboids and elevator scapulae)

long thoracic nerve (innervates the serratus anterior)

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34
Q

Trunks of the brachial plexus

A

Upper: C5-6

Middle C7

Lower C8-T1

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35
Q

cords of the brachial plexus: Lateral

A

named in reference to the axillary artery

Lateral (C5-7): gives rise to lateral pectoral nerve, median nerve, musculocutaneous

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36
Q

cords of the brachial plexus: Posterior

A

Posterior C5-T1: Gives rise to upper subscapular nerve, lower subscapular nerve, thoracodorsal nerve, axillary nerve, radial nerve

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37
Q

cords of the brachial plexus: Medial

A

C8-T1

medial pectoral nerve, medial brachial cutaneous nerve, medial antebrachial cutaneous + median, ulnar nerve

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38
Q

Familial amyloid polyneuropathy

mutation, inheritance

Type 1 vs Type 2

A

AD

transythretin mutation

Type 1: Polyneuropathy + autonomic features

Type 2: carpal tunnel syndrome, mild sensory polyneuropathy + absence of prominent autonomic features

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39
Q

CMT

features

nerve biopsy shows

A

heriditary sensorimotor polyneuropathy , high arched foot

onion bulb appearance

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40
Q

Demyelinating types of CMT

A

CMT1, CMTx, CMT4

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41
Q

CMT1

inheritance

mutation

features

CSF may show

A

AD (most common type)

DUPLICATION OF PMP22 on chromosome 17

hammertoes, high arched feet, palpably enlarged nerves and pes cavus

can see elevated protein in CSF

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42
Q

CMTx

inheritance

mutation

A

X linked

Connexion-32 gene

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43
Q

CMT2

inheritance

features

A

AD

axonal neuropathy (not demyelinating)

sx appear later in life, more UE than LE

can see optic atrophy (CMT2A), foot ulcerations, vocal cord paralysis, no peripheral nerve hypertrophy

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44
Q

CMT3 (Dejerine Sottas Syndrome)
features

A

most severe form, AD and AR

presents in infancy with proximal weakness, absent DTRs, hypertrophy of the peripheral nerves

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45
Q

HNPP (hereditary neuropathy with pressure palsy)

inheritance

mutation

features

biopsy

A

AD

deletion in PMP22

focal mononeuropathies (most commonly peroneal nerve, followed by ulnar nerve)

biopsy shows tomacula (myelin thickening)

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46
Q

Lesion in deep peroneal nerve presents with?

A

inability to dorsiflex (eversion is intact)

Superficial = eversion

Common = dorsiflexion and eversion

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47
Q

Foot drop + eversion impaired + inversion impaired ?

A

L5 radiculopathy

48
Q

Foot drop + eversion impaired + intact inversion?

A

common peroneal neuropathy

49
Q

Tangier’s disease

inheritance

features

unique PE finding

A

AR

defect with deposition of triglycerides causes sensory neuropathy with disassociated sensory loss (loss of pain and temp with preservation of the posterior column)

Deposition of TG can cause yellow/orange tonsils

50
Q

Anti-Hu is seen in some sensory neuropathies and is assoc with?

A

Small cell lung ca

51
Q

Anti-Yo is seen in some cerebellar degenerations and is assoc with?

A

ovarian ca

52
Q

Sciatic nerve gives rise to

A

tibial and common peroneal nerve

53
Q

Multifocal motor neuropathy (MMN)

features

AB assoc

treatment

A

purely motor demyelinating neuropathy, presents with asymmetric weakness from involvement of individual peripheral nerves + hypo/areflexia. no sensory deficits

anti-GM1

IVIG, no response to steroids or plasmapharesis

54
Q

Hypokalemic periodic paralysis

Inheritance

Types

presents with

triggered by

tx

A

AD

Type 1: Ca channel mutation (CACN), Type 2: Na channel (SCN4A)

presents with episodes of weakness without myotonia, during attack K is low.

exercise, carb high meals, alcohol, emotional stress, cold

diet + acetazolamide and K sparing diuretics

55
Q

Hyperkalemic periodic paralysis

inheritance

mutation

presents with

tx

A

AD
Sodium channel SCN4A

episodes of weakness triggered by exercise and fasting

can give glucose during attacks

tx with thiazides

56
Q

Anderson-Tawil Syndrome

mutation

features

A

K channel mutation in gene KCNJ2

periodic paralysis, ventricular arrhthymia, dystrophic features

57
Q

Paramyotonia

inheritance

mutation

features

A

AD

SCNA4

exercise induced myotonia most appreciated in the eyelids (in contrast to myotonia congenita)

58
Q

in steroid induced myopathy, there is atrophy of?

EMG? CK?

A

Type 2 fibers

EMG and CK nonspecific

59
Q

3 types of Anti-ACH Abs in MG

A

binding

blocking

modulating

60
Q

most common ACH Ab assoc with MG

A

binding (causing a complement mediated destruction of the receptor

61
Q

MOA of tensilon test

A

ACHesterase inhibitor = causes transient improvement of weakness

62
Q

Dystrophic myotonia Type 2 (aka proximal myotonic myopathy)

Inheritance, mutation

features

A

AD

CCTG repeat expansion in intron of zinc finger protein 9 gene on chromosome 3

myotonia of proximal muscles (type 1 is distal)

63
Q

Dystrophic myotonia Type 1

inheritance, mutation

features

A

AD

CTG repeat expansion in myotonic dystrophy protein kinase gene on chrom 1

myotonia of the distal muscles: ptosis, facial weakness, frontal balding, atrophy of the masters and temporals, weakness and atrophy of small muscles of the hands and extensor of the forearm and peroneal muscles, testicular atrophy, infertility, intellectual delay

64
Q

Facioscapulohumeral muscular dystrophy (FSHD)

inheritance, mut

features

A

AD

D4Z4 mutation on chromosome 4

  • Predominantly affects the face and shoulder
  • Presents with difficulty lifting their arms above their head with relative sparing of deltoid muscles + weakness of lower abdominal muscles (Beevor sign)
  • Forearm more atrophic than the arm—> Popeye
  • Weakness of foot dorsiflexion with preservation of plantar flexion is characteristic
65
Q

Symptoms that distinguish cholinergic crisis (pyridostigmine overdose) from myasthenic crisis

A

In pyridostigmine overdose: nausea, vomiting, diaphoresis sialorrhea, excessive bronchial secretions, mitosis, bradycardia and diarrhea

66
Q

Central core myopathy

inheritance, mut

features

pathology

A

AD
RYR1 (ryanodine receptor gene) on chrom 19

  • Can print with weakness and hypotonia after soon after birth and delay in motor development
  • Pelvic girdle more affected than shoulder girdle
  • Pathology: loss of oxidative activity of NADH within the center of muscle fibers (pale areas)
67
Q

Autonomic ganglionopathy

caused by

features

Ab

Tx

A

dysfunction in the parasympathetic and sympathetic nervous system

  • orthostatic hypoT, absent HR variability, hypo or anhidrosis, dry mouth and eyes, pupillary abnormalities, sexual dysfunctions, early satiety, constipation, and diarrhea due ti abnormal gastric and intestinal motility

may have Ab against ganglionic nicotinic ACH rec

PLEX and or IVIG

68
Q

In 50% of patients with clinic MG and Ab-ACH negative, what is pos

A

Anti-MUSK (muscle specific tyrosine kinase)

69
Q

Significance of Anti-MUSK (+) MG?

A

does not respond to pyridostigmine

70
Q

Features of congenital muscular dystrophies at birth?

A
  • hypotonic and weak, rest failure, bulbar dysfunction, scoliosis, developmental delay and anomaly of cerebral cortex causing seizures
71
Q

Pure autonomic failure (Bradbury-Eggleston Syndrome)

caused by

features

A

loss of intermediolateral cell column neurons, results in deposition of alpha-synuclein in autonomic nervous system (Lewy Bodies)

autonomic sx that are worse in the morning, after meals, with exertion and heat exposure

72
Q

What is seen in dermatomyositis and not seen in polymyositis

A

perifasicular atrophy

73
Q

Inclusion body myositis

features

pathology

A

myopathy affecting those >50yo

asymmetric weakness and atrophy of the wrist and finger flexors, quads, anterior tibial muscle → painless weakness that is distal leading to thumb flexing weakness with relative preservation of finger abductors (dorsal interossei)

Pathology: endomysial inflammation, intracytoplapmic vacuoles with granular material known as rimmed vacuoles

74
Q

Limb Girdle Muscular Dystrophy

features

assoc with

A

proximal weakness with involvement of shoulder or pelvic girdle with sparing of facial muscles

assoc with cardiomyopathy and conduction defects → need cardiac screening

75
Q

Difference between LEMS / MG

A

LEMS is less likely to have ocular or bulbar sx than MG

LEMS also more likely to have depressed DTRs

76
Q

Tx of LEMS? autoimmune LEMS

A

3,4 DAP (diaminopyridine)

steroids, IVIG, PLEX

77
Q

Nemaline myopathy

features

path

A
  • Proximal weakness, cardiomyopathy and prominent compromise of rest muscles

Fibers have rod like structures (nemaline rods)below the sarcolemma

78
Q

Pompe Disease (glycogen storage disease Type 2) is a deficiency of

A

Acid Maltase

79
Q

McArdles Disease (glycogen storage disease type 5) is a def of

A

myophosphorylase

80
Q

Cori’s Disease (glycogen storage disease Type 3) is a def of

A

glycogen debranching enzyme

81
Q

Congenital MG

caused by

features

difference in Tx from regs MG

A
  • Due to acetylcholine receptor deficiency
  • Most commonly present a birth (> males)
  • Typical presentation: ophthalmoparesis in infancy with facial diparesis
  • Not immune mediated, so not treated like MG
82
Q

Emery-Dreifuss muscular dystrophy

gene, inheritance

presents with

assoc with

A
  • AD, LMNA
  • Presents with contractures in elbows, ankles and neck.
  • Muscles weakness tends to affect the UE and shoulder girdle first and layer the pelvic girdle and distal legs
  • Cardiac involvement
83
Q

Difference between nerve structures (pre and post ganglion) in parasympathetic vs sympathetic

A

PARA: (ganglia are close to the target site) long pre and short post

SYMP: short pre and long post

84
Q

The neurotransmitter for all sympathetic and parasympathetic preganglionic fibers is _____ (acts on ____ receptors). Postgang in parasym release ______ while postgan in sympathetic release ________.

A

The neurotransmitter for all sympathetic and parasympathetic preganglionic fibers is acetylcholine (acts on nicotinic receptors. Postgang in parasym release acetylcholine while postgan in sympathetic release norepinephrine

85
Q

Autonomic system in the spine: Para vs symp

A

Parasympathetic - Onuf’s nucleus S2-S4 (GU and distal colon: controls the urethral and anal sphincters)

Sympathetic: intermediolateral cell column from T1-L2

86
Q

With lesion of the cauda equina, a flaccid bladder results from?

A

Loss of detrusor tone, sensation of bladder fullness is lost, voluntary control over urination is lost → overflow incontinence

87
Q

with lesions affecting the paracentral lobule (such as hydrocephalus or tumors), what is affected

A

voluntary control over the external urethral sphincter is lost

88
Q
  • Lesion above the conus medullaris lead initially to
A
  • a flaccid bladder leading to urinary retention with or without overflow incontinence.
89
Q

BUZZWORDS: acute onset dysautonomia in a smoker with a lung mass

A

Paraneoplastic autonomic ganglionopathy

Ab against ganglionic nicotinic ACH receptors

90
Q

BUZZWORDS: Duchenne muscular dystrophy (protein, inheritance)

A

dystrophin

X linked rec

91
Q

BUZZWORDS: tongue, ear, throat pain assoc with syncope

A

glossopharyngeal neuralgia

92
Q

BUZZWORDS: tilt table test showing inc in HR >30 from baseline, or more than 120 within 10 mins of head up tilt, without significant changes in BP but with sx of orthostasis

A

POTS

most common form of dysautonomia

93
Q

BUZZWORDS: Emery Dreifuss gene and inheritance

A

LMNA

AD

(could also be X linked and emerin

94
Q

BUZZWORDS: central core myopathy gene, path, assoc clinically

A

RYR1

central pare cores in NADH stains from absence of mitochondria

assoc with malignant hyperthermia

95
Q

BUZZWORDS: Tarul disease (enzyme)

A

phosphofructokinase def

96
Q

BUZZWORDS: cause of Hirschsprungs Disease

A

maldevelopment and absence of the myenteric plexus, sometimes due to RET proto-oncogene mutation

97
Q

BUZZWORDS: Becker’s muscular dystrophy protein, inheritance

A

abnormal or reduced dystrophin

XLR

98
Q

BUZZWORDS: syncope with hypotension and bradycardia after putting on a tight neck tie

A

carotid sinus hypersensitivity

99
Q

BUZZWORDS: Ab assoc with LEMS

A

presynaptic P/Q type voltage gated calcium channel antibodies

100
Q

BUZZWORDS: oculopharyngeal dystrophy (gene affected)

A

CTG repeat on PABP2 gene

101
Q

BUZZWORDS: pathologic finding in critical illness myopathy

A

myosin loss

102
Q

BUZZWORDS: Anderson’s disease (enzyme)

A

Branching enzyme deficiency

103
Q

ALS affects what parts of the brain

A

anterior horn cells, motor cortex, brainstem

104
Q

Split hand phenomenon in ALS?

A

weakness and atrophy of the lateral hand (thenar and FDI muscles) with relative sparing of the medial hand (hypothenar)

105
Q

Tx for psuedobulbar affect in ALS

A

dextromethorphan-quinidine

106
Q

What cognitive impairment is assoc with ALS?

A

FTD - have TDP-43(+) tau inclusion

107
Q

Familial ALS-FTD is assoc with what mutation?

A

C9ORF72 on chromosome 9

108
Q

Familial ALS mutation?

A

copper/zinc superoxide dismutase (SOD1) on chromosome 21

109
Q

Things usually spared in ALS?

A

bladder/sphincter issues - Onuf’s nucleus is spared

sensation

autonomic sx

110
Q

PLS (primary lateral sclerosis)

features

A

UMN signs at least 3 years from symptom onset wihtout evidence of LMN dysfunction. Presents in the 60s with progressive spastic tetraparesis and later cranial nerve involvement

111
Q

Most common cause of spinal cord involvement in patients with HIV

A

HIV-related myelopathy: vaculoar myelopathy in which there is lateral and posterior column demyelination with microvacuolar changes and axonal preservation (upper extremities typically spared)

112
Q

HTLV-1: tropical spastic paraparesis

features

MRI

labs

Tx

A

chronic progressive myelopathy endemic to equatorial and south Africa as well as parts of Asia, south america and caribbean. Transmitted via blood, sex, breast feeding.

p/w slow spastic paraparesis, LE paresthesias, painful sensory neuropathy and bladder dysfunction

MRI with inc T2 signal and atrophy of the thoracic cord

Dx with serum and CSF PCR

no tx at the moment

113
Q

Hereditary Spastic Paraparesis

inheritance, mut

features

A

AD

SPAST gene encoding spastin protein

Progressively worsening spasticity of the LE with variable weakness and difficulty walking

114
Q

What spinal levels are most susceptible to watershed injury?

A

T4-T8: blood supply is scarce

115
Q

Artery of Adamkiewicz: supplies and affected in

A

T8-L3 levels

can get infected in aortic arch dissection

116
Q

oculopharyngeal dystrophy: mutation

A

GCG repeat, PABP2 gene

117
Q

Duchenne MD
inheritance
mutation
features

A

X linked
dystrophin gene mutation
proximal muscles weaken with sparing of ocular, facial, bulbar

All should get cardiac checkup

Eugenie Notes (10 decks)

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