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Clin Med MSKII > Sachen Clinical > Flashcards

Sachen Clinical Flashcards

1
Q

EMG records what type of fibers

A

myelinated

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2
Q

Describe the fibers for Proprioception, Touch and pressure

A

type A, myelinated, big diameter, fast

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3
Q

describe fibers for Pain and Temp

A

Type C, unmyelinated, small diameter, slow

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4
Q

Most common nerve roots involved in Radiculopathy

A
  • C6 (C5-C6)
  • C6 (C6-C7)
  • L5
  • S1
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5
Q

what is part of the slcerotome for every cervical nerve root and thus there is pain here for each cervical radiculopathy

A

scapula

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6
Q

where is T1 dermatome

A

medial forearm . . there isn’t a T1 on chest

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7
Q

Sensory Symptoms of peripheral Nerve Disease

A
  • No loss of sensation
  • Paresthesias: secondary to large myelinated fiber disease (“pins and needles”)
  • Pain: secondary to small unmyelinated fiber disease (Burning, Dysesthesia-pain upon gentle tough, hyperalgesia- lower threshold to pain, hyperpathia- pain threshold is elevated, but pain is excessively felt)
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8
Q

Motor symptoms of peripheral Nerve Disease

A
  • distal weakness
  • cramps
  • muscle fasciculations (twitching)
  • Atrophy
  • DECREASED deep tendon reflexes
  • reduced tone
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9
Q

pain in shoulder and within a few days atrophy develops in deltoid and probably biceps and pain subsides . . inflammatory/idiopathic cause of brachial plexopathy

A

Parsonage Turner

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10
Q

Cause of plexopathy if there is history of cancer and treatment and it’s painless, lateral cord?

Painful, medial cord?

A

radiation injury

Neoplastic (breast or lung)

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11
Q

sensation to lateral calf and dorsum of foot EXCEPT flip flop zone

A

superficial fibular (peroneal) nerve

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12
Q

sites for median entrapment and mononeuropathy

A
  • wrist: carpal tunnel, sensory loss and thenar atrophy
  • Elbow: pronator teres syndrome, repetitive elbow motions
  • ligament of struthers
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13
Q

hand sensory distribution of median nerve

A

medial palmar surface, thenar eminence, 1st 2 and a half fingers

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14
Q

what is a key in distinguishing pronator syndrome from carpal tunnel syndrome

A

ABSENCE of nocturnal awakening because of pain or numbness . .this is typical of carpal tunnel

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15
Q

what median mononeuropathy gives you abnormal pinch sign

A

anterior interosseous syndrome

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16
Q

describe the nerve conduction studies with anterior interosseous syndrome

A
  • normal routine median and ulnar studies
  • abnormalities in needle EMG: FPL, FDP, PQ
  • other median, medial cord, C8 muscles are normal
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17
Q

Common sites of entrapment of ulnar nerve

A
  • Axilla
  • Elbow: b/t medial epicondyle and olecranon
  • Cubital tunnel: b/t tendinous arch of FCU
  • Wrist: Guyton’s canal
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18
Q

Froment sign

A
  • ulnar neuropathy

- have to flex thumb DIP joint to grip a piece of paper

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19
Q

Common sites of entrapment of Radial nerve

A
  • Axilla: Crutch palsy
  • Humerus/Spiral Groove: “Saturday night Palsy” . . most common
  • Supinator: posterior interosseous Branch
  • Wrist: superficial radial sensory branch
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20
Q

wrist drop

A

Radial nerve in spiral groove of humerus

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21
Q

sciatic nerve is what nerve roots

A

L4-S2

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22
Q

distribution for peripheral neuropathy

A

glove and stocking

-legs first and more severely than arms

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23
Q

CMT1 and 2 are hereditary neuropathies. Which one is demyelinating?
which is axonal?

A
  • 1

- 2

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24
Q

another name for Charcot-Marie tooth (CMT)?

A

Hereditary Motor Sensory Neuropathies (HMSN)

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25
Q

features of CMT1?

A
  • autosomal dominant
  • onset 1st or 2nd decade
  • often see difficultly walking or running first
  • distal symmetric atrophy (legs>arms)
  • arreflexia
  • mild sensory loss
  • skeletal deformities (pes cavus, HAMMER TOES, scoliosis)
  • EMG shows slowing of motor nerve conduction velocities (demyelination)
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26
Q

features of CMTII?

A
  • autosomal dominant
  • onset in adulthood
  • distal symmetric atrophy (legs>arms)
  • arreflexia
  • mild sensory loss
  • EMG shows normal or nearly normal motor nerve conduction velocities (axonal loss)
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27
Q

severe belly pain and polyneuropathy

A

porphyria: defect in heme biosynthesis

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28
Q

Orange tonsils and polyneuropathy

A

-Phytanic acid storage (Refsum’s) Disease

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29
Q

Acute inflammatory demyelinating polyneuropathy

A

Guillain-Barre Syndrome

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30
Q

what often precedes Guillain-Barre Syndrome

A
  • antecedent illness, surgery, immunization

- viral syndrome: Epstein-Barr, mycoplasma pneumonia, Campylobacter

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31
Q

symptoms of Guillain Barre Syndrome

A
  • low back/leg pain at onset
  • ascending usually symmetric weakness
  • hypo or absent DTRs
  • no/minimal sensory symptoms or signs
  • possible respiratory failure
32
Q

what are the key lab findings in Guillain Barre syndrome

A
  • CSF: albumino-cytologic dissociation (increase protein, normal cell count/normal glucose)
  • NCVs: slow conduction velocity, focal conduction block, prolonged F waves. focal spotty demyelination
33
Q

treatment of Guillain-Barre Syndome

A
  • supportive care

- Plasma exchange or IVIG

34
Q

describe the Miller fisher syndrome variant of Guillain Barre

A
  • ophthalmoplegia, ataxia, arreflexia
  • Facial weakness, dysarthria, dysphagia
  • GQ1b and GT1a antibodies
35
Q

time frame for Chronic inflammatory demyelinating polyneuropathy (CIDP)

A

->2months

36
Q

treatment for CIDP

A

-IVIG, steroids, plasma exchange, immunosuppressive agents

37
Q

clinical finding in multifocal motor neuropathy

A
  • adults
  • slowly progressive distal weakness of hands>feet
  • no sensory signs/symptoms, no UMN signs
38
Q

Lab findings in multifocal motor neuropathy

A
  • elevated serum GM-1 in 50-80%
  • EMG shows conduction block or demyelinating features
  • CSF normal
39
Q

treatment of Multifocal motor neuropathy

A

-IVIG

40
Q

cranial neuropathies associated with DM

A
  • CN III most common

- also VI and VII

41
Q

what are acquired axonal peripheral neuropathies usually from

A

toxins

  • DM
  • EtOH
  • uremia
  • CA
  • Metals
  • chemo
  • MM
42
Q

Hu antibody

A

carcinomatous sensory neuropathy

43
Q

anti MAG

A

MGUS

44
Q

aANCA

A

systemic vasculitis

45
Q

skin biopsy is done for what neuropathies

A

small fibeer

46
Q

metabolic cause of motor neuron disease. alpha-glucosidase (acid maltase) deficiency

A

pompe’s disease

47
Q

acquired motor neuron disease associated with asthma

A

Hopkins Syndrome

48
Q

highlights for ALS

A
  • no definite risk factors related to occupation, trauma, socioeconomic status
  • mixed upper (spasticity, hyperreflexia, Babinski sign) and lower (atrophy, fasciculations) motor neuron signs
  • may also be bulbar involvement of upper or lower motor neuron type
49
Q

pathophysiology of ALS

A

-degeneration of anterior horn cells and lateral and ventral corticospinal tracts

50
Q

age for ALS?

Characterized by?

A
  • b/t 20-60
  • degeneration of pyramidal (Betz) cells, anterior horn cells, brainstem motor nuclei of the lower cranial nerves, and corticospinal aand corticobulbar tracts
51
Q

Clinical presentation of ALS

A
  • gait disorder, limb weakness, speech or swallowing difficulty are common initial complaints
  • unexplained weight loss (due to loss of muscle bulk), cramps, and fascuculations
  • tongue atrophy and fasciculations commonly seen
52
Q

Diagnostic tests for ALS

A
  • EMG - widespread denervation and reinnervation
  • CPK - normal or slightly increased
  • CSF - normal
  • imaging studies of brain and spine- normal
  • muscle biopsy only in confusing cases
53
Q

important “Rule of thumb” diagnostic negatives for ALS

A
  • no sensory symptoms
  • normal mentation
  • No extraocular muscle involvement
  • bowel or bladder symptoms not prominent
  • Decubiti rare (ulcers from lying down)
54
Q

mean duration of symptoms for ALS

A

2-5 years

55
Q

highlights of progressive bulbar palsy

A
  • selective involvement of the motor nuclei of the lower cranial nerves
  • Dysarthria, Dysphagia, chewing difficulty, respiratory difficulty usual presenting features
  • often progresses to generalized involvement (ALS)
56
Q

highlights for progressive spinal muscle atrophy

A
  • mean age is 64
  • LOWER MOTOR NEURON deficits affecting the limbs due to degeneration of anterior horn cells
  • no upper motor neuron involvement
  • Weakness, atrophy, respiratory difficulty
  • can progress to ALS but usually does not
57
Q

highlights of infantile spinal muscular atrophy

A
  • Werdnig Hoffman Disease
  • hypotonia
  • arreflexia
  • poor suck
  • breathing difficulty
  • death in 6-12 months
58
Q

highlights for intermediate spinal muscular atrophy

A

-Chronic Werdnig Hoffman disease

59
Q

highlight for juvenile spinal muscular atrophy

A
  • Kugelberg-Welander Disease

- MIlder than Werdnig Hoffman

60
Q

What is a false transmitter in that it acts like Ca and can be taken up by the presynaptic Ca channel but doesn’t cause release of Ach

A

Mg

61
Q

caused by a defect of neuromuscular transmission due to an antibody-mediated attack upon nicotinic acetylcholine receptor (AChR) on muscle membrane

A

Myasthenia Gravis

62
Q

HLAs associated with Myasthenia Gravis

A

B8 and DR3

63
Q

what are the 3 general clinical characteristics of myasthenia Gravis

A
  • fluctuating weakness: “excessive fatigability”
  • Distribution of Weakness: ocular muscles (ptosis and diplopia), dysarthria, dysphagia, limb and neck weakness
  • clinical response to cholinergic drugs
64
Q

Lab finding for Myasthenia Gravis

A
  • anti AChR Ab’s
  • MUSK antibodies
  • EMG findings: decremental response on repetitive stimulation, increased “jitter” on single fiber EMG
  • Tensilon (edrophonium) test: watch for side effects
65
Q

Tensilon (edrophonium) test can cause what

A

HTN and cardiac arrhythmias so be careful and maybe hook up to EKG

66
Q

Treatment of Myasthenia Gravis

A
  • Acetylcholinesterase inhibitor
  • Prednisone
  • thymectomy
  • immunosuppressive agents
  • plasma exchange/ IVIG
67
Q

drugs that exacerbate or unmask myasthenia gravis

A

lots of them

-aminoglycosides most significant

68
Q

due to autoimmune attack against voltage gated calcium channels (VGCC’s) on presynaptic nerve terminal

A

-Lambert Eaton Myasthenic syndrome (LEMS)

69
Q

Lambert Eaton associated with what malignancy

A

Small cell cancer of lung

70
Q

Clinical Presentation of Lambert Eaton that distinguish it from Myasthenia Gravis

A
  • LOSS of DTRs (MG usually preserved)
  • Dry mouth and impotence (autonomics)
  • Strength may improve after exercise
71
Q

Treatment of Lambert Eaton

A
  • first look for and treat malignancy
  • Actylcholinesterase inhibitors
  • 3-4 Diaminopyridine
  • Guanidine hydrochloride
72
Q

what does Botulism toxin block

A

presynaptic mechanisms for release of ACh

73
Q

clinical presentation of Botulism

A
  • dry, sore mouth and throat
  • blurred vision
  • diplopia
  • nausea
  • vomiting
  • hypohydrosis
  • total external ophthalmoplegia
  • facial, oropharyngeal, limb and respiratory paralysis
74
Q

treatment of botulism

A

-ICU monitoring with respiratory support and general medical care

75
Q

what is a common symptom of Nerve Gas exposure (Sarin and VX) that you don’t see in MG or lambert eaton

A

Miosis (pupil involvement)

76
Q

if somone comes in with lambert eaton and has migraine headaches are you going to give Mg for headaches?

A

no . . can make lambert eaton worse

77
Q

if someone comes in with MG or lambert eaton and its getting worse and they have to take more ACheI’s how do you tell if its the disease or medication

A

-if you see fasciculations, increased secretions, diarrhea and abdominal cramps then ACh overload from meds

Clin Med MSKII (16 decks)

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