NM Flashcards

1
Q

Define recruitment. What conditions is it decreased in?

A

firing frequency of the first motor unit when a second motor unit is recruited.
-decreased in ALS, radic, PN.

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2
Q

Define MUAP. What conditions is it increased and decreased in?

A

spikes of electrical activity reflecting number of motor unit (motor neurons and muscle fibers they transmit to) activated when the patient voluntarily contracts a muscle.

  • Increased in ALS, chronic radic and chronic axon loss.
  • Decreased in myopathies.
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3
Q

What drug is bad for MG with intubation? How reverse? What should be used instead?

A

Curonium is bad.
Reverse with sugammadex.
Can use inhaled fluranes instead.

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4
Q

What is seen on muscle histology with steroid use?

A

type II muscle fiber atrophy

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5
Q

What type of myopathy do statins cause?

A

necrotic and inflammatory

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6
Q

Definition of CIDP v AIDP timeline. What is the role of steroids in these conditions?

A
  • CIDP continues to progress or has relapses for > 4 wks, AIDP reaches nadir at 3-4 wks.
  • Steroids make AIDP worse, used to treat CIDP.
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7
Q

Difference between myasthenic crisis and cholinergic crisis

A
  • myasthenic: defined as MG c/b RF requiring intubation. Happens in 20% patients. Triggers are infection, aspiration, trauma, childbirth, decrease in MG meds, reduction of other IS meds, Botox injections, meds (esp fluoroquinolones, amino glycosides, beta blockers, CCBs)
  • cholinergic: overmedication w cholesterase drugs (too much parasympathetic muscarinic-abd pain, diarrhea, vomit and nicotinic-bronchial and nasal secretions, etc)
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8
Q

When do you intubate/BiPAP a MG patient?

A

VC<10 ml/kg or

NIF < 20 (how much patient can suck in)

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9
Q

MG paraneoplastic (thymoma) in ___% cases. .

A

10-15% Surgical resection is treatment.

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10
Q

Lower limit of normal nerve conduction in BUE, BLE.

A

UE 50 m/sec, LE 40m/sec

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11
Q

Kennedy syndrome and inheritance pattern

A

Bulbar weakness, fasciculations, gynecomastia

-CAG trinucleotide repeat

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12
Q

Multifocal motor n uropathy (With conduction block)

A
  • subacute onset of asymmetric weakness and LMN signs of arm and hand weakness without assoc sensory loss, patchy nerve involvement, often decr or absent reflexes in affected limb(s)
  • Rx with steroids or IVIG
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13
Q

IVIG dose

A

2g/kg over 2-5d (ie 0.4 g/kg daily for 5d)

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14
Q

CMT inheritance pattern

A

duplication, PMP22

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15
Q

Nonaka myostits

A
  • distal myopathy in young ppl

- often p/w only TA inv (foot drop)

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16
Q

paraspinal muscles are innervated by ___

A

dorsal rami directly off the spinal nerve roots

17
Q

How long does reinnervation take to see on EMG?

A

3 mo

18
Q

What indicates active denervation on an EMG?

A

fibrillation potentials and positive sharp waves (can also be seen in some myopathies and severe NMJ disease.

19
Q

Changes in NCS if < 32 degrees C

A

increase latency, CV, amplitude, duration of responses

20
Q

F response

A

motor response after CMAP, no synapse, all nerves in pathway are motor

21
Q

H reflex

A
  • S1 reflex, stimulates the tibial nerve
  • afferent is sensory/efferent is motor
  • abnormal in tibial/sciatic neuropathy, sacral plexopathy, S1 radiculopathy, sensory neuropathy
22
Q

rapid repetitive stimulation in LEMS causes what on EMG?

A

facilitation in CMAP

23
Q

“machine like” sound on EMG

A
  • complex repetitive discharges (single muscle fiber depolarizing spreading to other denervated fibers)
  • chronic neuropathic and myopathic d/o
24
Q

“corn popping” sound on EMG

A
  • fasciculations
  • spontaneous discharge of individual motor unit*
  • seen in motor neuron disease, radiculopathy, polyneuropathy, entrapment neuropathy, benign fasciculation syndrome.
25
Q

“marching soldiers” sound on EMG

A

-myokymia (like grouped firing of same motor unit whereas tremor is different motor units.)

26
Q

What are EMG findings in a myopathy?

A

polyphasia, early MUAP recruitment, decreased amplitude of MUAP, short duration and low amplitude. If there is muscle fiber necrosis may see abnormal spontaneous activity.

27
Q
Evolution of axonal loss on EMG:
<3d (hyperacute)
1wk - 3/6wks (acute)
3/6 wks - 2/3mos (subacute)
>2/3mos - many mos/y (subacute - chronic)
many yrs (chronic)
A

hyperacute - normal NCS, EMG with decr MUAP recr

acute - NCS: decr sensory and motor amp, normal CV and distal latency. EMG: +/- spontaneous activity in proximal muscles, decr MUAP recr

subacute - same as acute

chronic - NCS: same as acute although may be normal. EMG: decr MUAP recr, abn MUAP morphology (d/t reinnervation), no abnormal spontaneous activity

28
Q

NCS in acquired v hereditary demyelination

A

Acquired: conduction block*
Hereditary: NO conduction block*

Rest is the same: prolonged/increased distal latencies, slow/decreased conduction velocity

29
Q

EMG and NCS in CNS d/o

A

EMG: decreased activation
NCS: normal

30
Q

When does wallerian degeneration start?

A

motor nerves: day 3-5

sensory nerves: day 6-10

31
Q

Carpal tunnel exam

A

weakness in thumb opposition and adduction, thenar eminence wasting, decreased sensation in digits 1-3 and lateral 4th.

32
Q

Anterior interosseous mononeuropathy exam

A

-trouble making ‘ok’ sign
-weakness of flexor pollicus longus, flexor digitorum profundus (2-3) and pronator quadratus
(weakness in flexing distal thumb, index and middle finger and pronation with arm flexed.)
-no sensory loss