NM Flashcards
Define recruitment. What conditions is it decreased in?
firing frequency of the first motor unit when a second motor unit is recruited.
-decreased in ALS, radic, PN.
Define MUAP. What conditions is it increased and decreased in?
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.
What drug is bad for MG with intubation? How reverse? What should be used instead?
Curonium is bad.
Reverse with sugammadex.
Can use inhaled fluranes instead.
What is seen on muscle histology with steroid use?
type II muscle fiber atrophy
What type of myopathy do statins cause?
necrotic and inflammatory
Definition of CIDP v AIDP timeline. What is the role of steroids in these conditions?
- 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.
Difference between myasthenic crisis and cholinergic crisis
- 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)
When do you intubate/BiPAP a MG patient?
VC<10 ml/kg or
NIF < 20 (how much patient can suck in)
MG paraneoplastic (thymoma) in ___% cases. .
10-15% Surgical resection is treatment.
Lower limit of normal nerve conduction in BUE, BLE.
UE 50 m/sec, LE 40m/sec
Kennedy syndrome and inheritance pattern
Bulbar weakness, fasciculations, gynecomastia
-CAG trinucleotide repeat
Multifocal motor n uropathy (With conduction block)
- 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
IVIG dose
2g/kg over 2-5d (ie 0.4 g/kg daily for 5d)
CMT inheritance pattern
duplication, PMP22
Nonaka myostits
- distal myopathy in young ppl
- often p/w only TA inv (foot drop)
paraspinal muscles are innervated by ___
dorsal rami directly off the spinal nerve roots
How long does reinnervation take to see on EMG?
3 mo
What indicates active denervation on an EMG?
fibrillation potentials and positive sharp waves (can also be seen in some myopathies and severe NMJ disease.
Changes in NCS if < 32 degrees C
increase latency, CV, amplitude, duration of responses
F response
motor response after CMAP, no synapse, all nerves in pathway are motor
H reflex
- S1 reflex, stimulates the tibial nerve
- afferent is sensory/efferent is motor
- abnormal in tibial/sciatic neuropathy, sacral plexopathy, S1 radiculopathy, sensory neuropathy
rapid repetitive stimulation in LEMS causes what on EMG?
facilitation in CMAP
“machine like” sound on EMG
- complex repetitive discharges (single muscle fiber depolarizing spreading to other denervated fibers)
- chronic neuropathic and myopathic d/o
“corn popping” sound on EMG
- fasciculations
- spontaneous discharge of individual motor unit*
- seen in motor neuron disease, radiculopathy, polyneuropathy, entrapment neuropathy, benign fasciculation syndrome.
“marching soldiers” sound on EMG
-myokymia (like grouped firing of same motor unit whereas tremor is different motor units.)
What are EMG findings in a myopathy?
polyphasia, early MUAP recruitment, decreased amplitude of MUAP, short duration and low amplitude. If there is muscle fiber necrosis may see abnormal spontaneous activity.
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)
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
NCS in acquired v hereditary demyelination
Acquired: conduction block*
Hereditary: NO conduction block*
Rest is the same: prolonged/increased distal latencies, slow/decreased conduction velocity
EMG and NCS in CNS d/o
EMG: decreased activation
NCS: normal
When does wallerian degeneration start?
motor nerves: day 3-5
sensory nerves: day 6-10
Carpal tunnel exam
weakness in thumb opposition and adduction, thenar eminence wasting, decreased sensation in digits 1-3 and lateral 4th.
Anterior interosseous mononeuropathy exam
-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
