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NEUROMUSCULAR > lecture 3 GD- nueromuscular > Flashcards

lecture 3 GD- nueromuscular Flashcards

1
Q

what are the 4 components of the peripheral nervous system

A
  • neuron cell body
    -peripheral processes
    -neuromuscular junction
    -mm
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2
Q

in the neuron cell body what is sensory and what is motor

A

dorsal root ganglion is sensory and anterior horn cell is motor

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3
Q

what type of fibers function as dull , aching , burning pain and temperature sensation

A

C

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4
Q

what type of fiber function as sympathetic preganglionic motor axons

A

B

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5
Q

what type of axon fiber functions as shap pain ,very light touch and temp sensation

A

ad

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6
Q

what type of axon fiber functions as touch, pressure , vibration and joint position sensory axons

A

aB

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7
Q

what type of axon fibers functions as large motor axons , mm stretch and tension sensory axons

A

Aa

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8
Q

what is a Progressive fatal disease associated with degeneration of upper and lower motor neurons

A

ALS

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9
Q

is ASL more common in men or women

A

men

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10
Q

what is the avery life expectancy of people with ALS

A

3 years from time of diagnosis

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11
Q

what are LMN signs of people with ALS

A

weakness, atrophy and fasciculations

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12
Q

what is UMN signs of ppl with ALS

A

pathologic spread fo reflexes , clonus

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13
Q

what is the most common genetic causes for ALS

A

C9orf2 hexanucleotide

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14
Q

what does C9orf72 hexanucleotide also cause

A

frontotmeporla dementia

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15
Q

what is the main symptom for LAS

A

fatigue and mm stiffness

(fatigue is the most tho)

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16
Q

what are the 3 FDA approved medications for ALS

A

• Riluzole
• Edaravone
• Tofersen

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17
Q

what is the symptom management fro faitgue in ALS patients

A

BIPAP, Modafinil

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18
Q

what is the symptom management for mood in ALS patients

A

SSRI’s

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19
Q

what is the symptom management for Pseudobulbarpalsy(PBA) in ALS patients

A

Nuedexta

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20
Q

what has been associated with an increased risk of ALS

A

intense physical activity

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21
Q

what is anarthropod-borne flavivirus

A

west nile virus

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22
Q

how does the west nile virus transmission occur

A

following a bit from an infected mosquito which got the virus after feeding on other hosts , mainly birds

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23
Q

when is the e peak transmission for west nile virus

A

july-octovober

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24
Q

are people with the west nile virus symptomatic or asymptomatic

A

80% are asymptomatic

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25
Q

what is the west nile fever

A

myalgia, headache, fever, and maculopapular rash)

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26
Q

Less than 1% of west nile virus cases are ____

A

neuroinvasive

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27
Q

what are the 3 things that can happen if the west nile virus is neuroinvasive

A

– Aseptic meningitis
-Meningoencephalitis(including brainstem encephalitis)
– Acute flaccid paralysis

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28
Q

acute flaccid paralysis is an acute onset and rapid progression of what 2 things

A

-asymmetric flaccid weakness and hypo active/absent reflexes

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29
Q

what other 2 things can happen with acute flaccid paralysis

A

-respiratory insufficiency
-bowel and bladder dysfucntion

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30
Q

Poliovirus is anRNA Enterovirus that belong to the ___ family

A

Picornavirus

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31
Q

Most poliovirus infections are ___,with viral growth limited to the ___

A

asymptomatic

gut

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32
Q

if someone had a minor disease of polio what would happen

A

flue like illness due to viremia

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33
Q

what is the diagnostic criteria for post polio syndrome

A
  1. History of paralytic poliomyelitis
  2. period of partial or complete recovery followed by interval of stable function
  3. gradual or sudden onset of progressive and persistent mm weakness
  4. symptoms for > 1year
  5. exclude other casues
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34
Q

what is the neurological examination of post polio syndrome

A

-LMN syndrome
- joint pain and cold intolerance may happen

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35
Q

t/f some people may have new neurologic problems unrealted to polio for post poli syndrome

A

T

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36
Q

each nerves root corresponds to a ___ and ___

A

dermatome and myotome

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37
Q

what is an area of skin supplied by a particular nevre root

A

dermatome

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38
Q

what is a myotome

A

mm inverneated by a particular nerve root

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39
Q

what are symptoms of radiculopathy

A
  • pain , numbness and thingling in the corresponding dermatome
    -weakens of mm supplied by the corresponding myotome
  • reduced reflex
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40
Q

if C7 root is causes neurologic S&S which disc is it compressed in

A

C6-C7

for the cervical spine it is always the one above the root

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41
Q

if a patient has pain in the low back , buttock , and later high and you found sensory finding in her lateral leg , dorosmedial foot and large toe and the motor finding were tight adduction , knee flexion and DF what root would u suspect is damaged and between what disc

A

L5 and between L4-L5

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42
Q

if your patient has pain in the medial forearm and hand and 5th digit and u find sensory finding at the medial forearm and hand and 5th digit and motor finding in the intricinc hand mm and a finger flexor change in reflex what nerve root would u suspect and between which disc

A

c8 and c7-t1

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43
Q

if your patient has pain int he dorsal forearm area and u find sensory changes int he 3rd and 4th fingers and motor fingers in arm extension , finger and wrist flexors and extensors and a reflex change in the triceps would root would u suspect and in between which disc

A

C7 and C6-C7

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44
Q

how do u treat radiculopthy

A

improve with time and pt

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45
Q

___ of cervical radiculopathies due to herniated disk improve without surgical intervention.

A

95%

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46
Q

when do u get sx for radiculopathy

A

– Not responding to PT
– Intractable pain
– Significant weakness

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47
Q

how do u differentiate between radiculopathy and lower motor neuron lesion

A

A – weakness
B – radicular pain in a dermatomal distribution
C – muscle atrophy
D – hyporeflexia

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48
Q

what is it called when Mutiple spinal nerve roots effected

A

polyradiculopathy

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49
Q

what are the S&S of polyradiculopathy

A

Motor symptoms predominate, variable degree of sensory loss, pain, generalized loss of DTRs

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50
Q

Inflammatory (Guillan-Barre, sarcoid, SLE, Sjogrens), DM, porphyria, Infectious (lyme, HIV, VZV, CMV, TB), neoplastic.. these are all etiologies of what

A

polyradiculopathy

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51
Q

what plexi is plexopathy effected

A

cervical or lumbosacral

52
Q

what are S&S of plexopathy

A

pain , restricted to single limb , more widespread then single nerve or root

53
Q

what are the casues/etiologies of plexopathy

A

trauma most common , malignant infiltration , thoracic outlet syndrome

54
Q

what is Neuropathy of single peripheral nerve

A

mononeuropahty

55
Q

what are the sings of mononeuropahty

A

restricted to anatomic distribution of one nerve

56
Q

what is the causes of mononeuropahty

A

compression , entrapment , trauma

57
Q

carpal tunnel and meralgia parasthetica are examples of what

A

mononeuropahty

58
Q

what is carpal tunnel

A

median never compressed at the wrist

59
Q

what is meralgia parasthetica

A

lateral femorla cutaneous compressed at inguinal ligament

60
Q

what is polyneuropathy

A

generalized process affecting peripheral nerves

61
Q

whar are signs of polyneuropathy

A

commonly symmetric , length dependent weakness, sensory loss, loss of DTRs (stocking glove distribution so from distal to proximal)

62
Q

• Sensory, Motor, Autonomic
• Large fiber, small fiber
• Demyelinating, Axonal
• Hereditary, Acquired

this would characterize what

A

polyneuropathy

63
Q

Most of the myelinated fibers are ____ diameter fibers

A

LARGE

64
Q

what are suggestive features of demyelinating

A
  • Weakness without atrophy
  • Length independent
  • Patchy
  • Asymmetric
65
Q

• Compression/stretch
• Guillain–Barresyndrome
• ChronicInflammatoryDemyelinatingPolyneuropathy(CIDP)
• Multifocal motor neuropathy
• Diphtheria
• Charcot – Marie – Tooth
• Hereditary neuropathy with liability to pressure palsies
• MAG-neuropathy
• Leukodystrophies
• Diabetes

these are all examples of what

A

Demyelinating

66
Q

what are suggestive features of axonal demyelinating

A

– Distal>proximal
– Legs>arms(longer axons more susceptible)
– Muscle wasting early

67
Q

*
Diabetes
AMAN / AMSAN (axonal GBS)
Toxic – vincristine, acrylamide, arsenic
Alcohol
Uremia
Collagen vascular diseases
Carcinoma
Amyloid

these are examples of what kind of neuropathy

A

axonal

68
Q

small diameter never fibers that are sensory carry information about __ and ___

A

pain and temp

69
Q

what are 2 nerves that are small diameter nerve fibers

A

sensory never and autonomic

70
Q
  • Reduced ability to feel pain and hot/cold temperature
  • Allodynia
  • Burning, electric current-like, neuropathic pain
  • Discoloration of the skin, reduced sweating in the feet, loss of hair in the feet/legs
  • Autonomic dysfunction

patients that present with this will have what type of nerupathy

A

small fiber

71
Q

what are the 2 nevers that are large diameter nerve fibers

A

motor and sensory nerves

72
Q

large diameter nerve fibers that are sensory nerves carry information about ___, ____ and ____

A

pressure , vibration and proprioception

73
Q

neuropathy that affects the large fibers present with what

A

• Numbness, tightness, balance problem
• “walking on foam, cobblestone

74
Q

autonomic neuropathy is an autonomic dysfunction that is ____

A

involuntary

75
Q

what are the 5 S&S of autonomic neuropathy

A
  • orthostatic hypotension
  • arrthymias
    -severe constipation , urinary retention and erectile dysfunction
  • sweating
  • early satiety , lightheadedness with meals
76
Q

– Diabetes or IGT(Impaired Glucose Tolerance)
– Thyroid disease (hypo or hyperthyroidism)
– Toxic (alcohol, chemotherapy agents, HIV medications, heavy metals)
– Vitamins and/or nutritional deficiencies (vitamin B12, B6, vitamin E, Copper, Zinc)
– Systemic Conditions (kidney problems/cancers/autoimmune)
– Infections: HIV, Syphilis, Lyme, Herpes
– Immune mediated (CIDP, GBS)

theses are major causes of what

A

polyneuropathies

77
Q

inflammatory demyelinating polyneuropathies is a disorder that causes what

A

weakness, sensory loss and areflexia

78
Q

what is a rapidly progressive inflammatory demyelinating polyneuropathy and when does pression end

A

acute inflammatory demyelinating polyneuropathy ( AIDP or guillain- barre syndrome)

progression ends by 4 weeks

79
Q

what is a slowly progressive inflammatory demyelinating polyneuropathy and when does pression end

A

• Chronic inflammatory demyelinating
polyneuropathy (CIDP)
• Weakness progressing > 2 months

80
Q

what is the progression for Acute Inflammatory Demyelinating Polyneuropathy

A
  1. tingling , parasthesia w little sensory loss
  2. severe radicualr back pain
  3. weakness
    - legs and arms
    -legs then arms
    -arms to legs
    -facial (most common)
    -dysphagia
81
Q

what does the exam for Acute Inflammatory Demyelinating Polyneuropathy (gullian barre syndrome) show

A

mostly symmetric weakness
- areflexia in most after 1 week

82
Q

what is absence and what is elevated when doing a CSF with albuminocytologic dissociation in someone with Acute Inflammatory Demyelinating Polyneuropathy (gullian barres)

A

no WBC’s and elevated protein

83
Q

what hasten recovery for people with guillain barre syndrome

A

plasma exchange and IVIG

84
Q

T/F: steroids are beneficial for guillain barre syndrome

A

F

85
Q

is Chronic Inflammatory Demyelinating Polyneuropathy more common in men or women

A

men

86
Q

Chronic Inflammatory Demyelinating Polyneuropathy is _____ progressive sx over weeks–months

A

Slowly

87
Q

does Chronic Inflammatory Demyelinating Polyneuropathy affect more motor or sensory

A

motor

88
Q

is symmetric weakness proximal and distal more common or atrophy in Chronic Inflammatory Demyelinating Polyneuropathy

A

symmetric

89
Q

where is sensory loss mainly from Chronic Inflammatory Demyelinating Polyneuropathy

A

legs

90
Q

diabetic neuropathies is a ____ ____ pattern in polyneuropathy

A

length dependent

91
Q

does biabetic neuropathies affect LE or UE first

A

LE (stocking glove sensory loss)

92
Q

does diabetic neuropathies causes weakness ?

A

no

93
Q

what is associated with less frequent and less severe neuropathy

A

tight glucose control

94
Q

– Tricyclic antidepressants -> Cymbalta
– Gabapentin -> Lyrica
– Tramadol
– Topical capsacin

these al treat neuropathic pain in what

A

diabetic neuropathy

95
Q

Diabetic Lumbosacral Radiculoplexus Neuropathy (DLRPN) aka Diabetic Amyotrophy is usually in type 1 or type 2 diabetes

A

2

96
Q

**Diabetic Lumbosacral Radiculoplexus Neuropathy (DLRPN) aka Diabetic Amyotrophy is associated with ___ weight loss and beings ____

A

large and abruptly

97
Q

Diabetic Lumbosacral Radiculoplexus Neuropathy (DLRPN) aka Diabetic Amyotrophy being with what

A

sharp or aching pain asymmetrically in the hip and thigh which can spread to the leg and foot

98
Q

in Diabetic Lumbosacral Radiculoplexus Neuropathy (DLRPN) aka Diabetic Amyotrophy how does weakness progress

A

distally and can become bilateral

99
Q

Insidious onset, indolent course, onset <20 years old is present in what

A

hereditary neuropathy

100
Q

what is the term used to describe group genetic neuropathies

A

charcot marie tooth disease

101
Q

what are 2 clinical manifestions of Charcot-Marie-Tooth Disease

A

distal weakness and atrophy and length dependent sensory loss

102
Q

what foot deformities are present with Charcot-Marie-Tooth Disease

A

pes cavus , pes plannus , hammer toes

103
Q

how are the reflexes in Charcot-Marie-Tooth Disease

A

absent or decreased

104
Q

does Charcot-Marie-Tooth Disease progress slow or fast

A

slow

105
Q

– Delayed early milestones
– Slow progression
– Absence of positive sensory symptoms but
prominent sensory loss on exam
– Foot deformities, injuries, surgeries
– Family history/consanguinity
– Hip problems/scoliosis

would this make u think hereditary or acquired

A

hereditary

106
Q

what is the early onset of Charcot-Marie-Tooth Disease

A

-delayed onset of walking
-very slow CV

107
Q

what is the childhood onset for Charcot-Marie-Tooth Disease

A
  • normla walking
    -slow runner as child
  • develop symptoms 5-20 years old
  • most common
108
Q

what are presynaptic disorder of the neuromuscular junction

A

– Lambert Eaton myasthenic syndrome
– Botulism

109
Q

what is a **post synaptic **disorder of the neuromuscular junction

A

Myasthenia gravis

110
Q

– Fluctuating, fatigable
– Asymmetric ptosis, diplopia
– Difficulty chewing
– Dysarthria, dysphagia, nasal speech
– Hoarseness
– Head drop
– Limb weakness

if someone presents with this int he clinic what do they have

A

myasthenia gravis

111
Q

myasthenia gravis is a ___ disorder

A

autoimmune

112
Q

what are 7 triggers fro MG

A

• Emotional upset
• Viral illnesses and other systemic illness, fever
• Heat
• Hypo or hyperthyroidism
• Surgery
• Menstrual cycle
• Drugs

113
Q

– D-penicillamine
– IFN-α,
– Botox
– Succinylcholine
– Magnesium salts

these are drugs that should never be used for what

A

Myasthenia gravis

114
Q

what test for u do for myasthenia gravis dianosis

A

tensilon test

115
Q

what are negative signs for myopathies

A

• Weakness
• Fatigue
• Atrophy
• Exercise Intolerance

116
Q

what are positive symptoms for myopathies

A

• Myalgia
• Cramps
• Contractures
• Hypertrophy
• Stiffness
• Myoglobinuria

117
Q

what will we see for a physcial exam for myopathy

A
  • proximal weakness
    -sensation intact
  • DTR can be normal or little reduces
118
Q

• MuscularDystrophies
• Congenital Myopathies/Muscular Dystrophies
• Metabolic/Mitochondri al
• Channelopathies

are these classification of hereditary or acquired myopathies

A

hereditary

119
Q

what are acquired myopathies

A

• Toxic/DrugInduced
• Endocrine
• Inflammatory/Immune
• Associatedwith Systemic Illness

120
Q

Polymyositis and dermatomyositis is a chronic onset of ___ weakness and has variable ___ and ___ invovlment

A

proximal
cardiac and pulmonary

121
Q

Polymyositis and dermatomyositis can be

A

malignancy (eso dermatomyositis)

122
Q

MTX and Azathioprine are apart of what treatment line for dermatomyositis

A

2nd line

123
Q

what is the management for dermatomyositis

A

• Cancer Screening
• Bone Health while on steroids
– Calcium & Vitamin D
• Physical Therapy

124
Q

what is the most frequent myopathy in patients >50 and more common in men

A

inclusion body myositis

125
Q

is inclusion body myositis slow or fast progressive weakness

A

slowly

126
Q

how will the weakness present in inclusion body myositis

A

proximal left and distal arm
-asymmetric
-mm atrophy
-dysphagia

NEUROMUSCULAR (15 decks)

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