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29 Cards in this Set

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Components of ncs

CMAP: VLAD (velocity, latency, amplitude, duration)


SNAP: VLAD (use peak latency)

How to distinguish axonal vs demyelination

Axonal: amplitude affected > velocity


Demyelinating: velocity > amplitude

5 features of demyelination on ncs

Conduction block: drop in CMAP amplitude of 50% (proximal normal, but distal low)


Temporal dispersion: > proximal CMAP duration is 30% greater than distal CMAP (30% more spread out)


slowed conduction Velocity: decreased by 30% (70% of normal)


prolonged Distal latency: > = 50% of ULN (150% of normal cutoff)


absent/delayed F waves:

Amplitude, 3 velocity (temporal dispersion, CV, DL), F waves, HINT: CTV DF

Define f response, h response, a reflex

F response: late motor response due to antidromic travel to anterior horn cell which bounces back along nerve, variable since different anterior horn cell stimulated each time.


H response: electrical correlate of tendon reflex (sensory to motor)


A reflex: small motor response after CMAP due to reinnervation (travels along collateral axon

Martin Geiger anastamosis

crossover of motor fibers from median to ulnar nerve in forearm. In 15-30% ppl


Median nerve will innervate ulnar muscles (ADM, FDI) and will look like ulnar conduction block

EMG components

Spontaneous activity:


muscle fiber: fibrillations, PSW, CRD, myotonic discharge (FPCM)


motor unit/axon: fasciculation, doublet/triplet, myokimia, cramp, neuromyotonia (FDMDN)


Voluntary activity: MUAP morphology: amplitude, duration, polyphasia, recruitment

EMG: neurogenic vs myopathic

Neurogenic: decreased recruitment, MUAPs are large amplitude, long duration, polyphasic


Myopathic: early recruitment, MUAPs are small amplitude, short duration, polyphasic

Timing of ncs/EMG changes in acute Adonai lesion

Acute <1wk, early recruitment, otherwise normal


10-14d-wallerian degeneration = smaller CMAPs


1 month: abn spontaneous activity: fibs/PSW


2 months: large MUAPs


Months-years: large MUAPs/decreased recruitment, CMAP may improve and spontaneous activity may resolve

Hint: recruitment, CMAP, spontaneous activity, MUAP (1 wk/2wk/1mo/2mo)

Ddx of Anterior horn cell disease

ALS, SMA1-3, Kennedy’s disease (x linked spinobulbar atrophy)


Infectious: polio, post polio, WNV, HIV, HTLV-1


Toxic: lead, arsenic, thallium


Other: delayed radiation induced MND, paraprotein related motor neuropathies, monomelic amyotrophy

ALS diagnostic criteria

El Escorial criteria: combo of UMN and LMN in 4 areas (bulbar, cervical, thoracic, lumbar)


a) evidence on LMN degeneration (clinical or electrophysiological)


b) evidence if UMN degen


c) progressive spread


e) electrophysiology does not indicate another process


d) imaging does not indicate another process


definite (3 regions), probable (2 regions), suspected (1 region)

ALS vs MMN

distribution of weakness, MMN is nerve, ALS is myotomal


UMN findings only in ALS


Bulbar weakness: in ALS not MMN


NCS: demyelination in MMN, ALS often normal or reduced CMAPs


EMG: ALS has more evidence of active denervation (fibs/PSW), involves paraspinals


labs: antiGM1 in MMN

Genetics of ALS

Genetics of ALS


5-10% are genetic (AD): C9ORF72 (30%), SOD1 (20%), TDP 43 (10%), FUS (5%)

ALS treatment

riluzole


- Edaravone: free radical scavenger. Overall analysis no benefit but subgroup analysis showed reduction of functional decline by 1/3 in those at earlier stage/milder disease (FVC> 80%, scoring 2+ points on all items on ALSFRS and disease duration <2yrs and moderate rate of progression)

Kennedy’s disease: features and genetics

progressive limb and bulbar weakness, perio-oral fasic, gynecomastia, testicular atrophy/impotence/infertility, mild sensory neuropathy


X linked androgen receptor gene, CAG expansion

SMA: genetics and subtypes

SMA: explain the genetics and subtypes


AR, deletion of the SMN1 gene (survival motor neuron) on chromosome 5


variable # of SMN2 genes determines SMA 1-3


SMA 1 (1 or 2 copies SMN2) never sit, death by age 2


SMA2 (3 copies SMN2) never walk, onset 6-18mo


SMA3 (4 copies SMN2) never run, onset 5-15yo

List parts of brachial plexus

Roots (C5-T1) =>


trunk (UML) =>


division =


cords (lateral/post/medial

Features of the 3 trunks and 3 cords of brachial plexus

Trunks: Upper: C5/6, Middle: C7, Lower: C8/T1


Cords:


Lateral cord contributes to MSC and median


Posterior: subscapular (teres major), thoracodorsal (lats), axillary and radial


Medial: Medial cut of arm/forearm, median, ulnar

Distinguish: upper trunk (C5/6) vs lateral cord

lateral cord spares


axillary


suprascapular (supra/infraspinatus)


C6 radial (brachiorad)

Brachial plexopathy ddx

trauma, neoplasm, radiation, diabetes, parsonage Turner syndrome

Radiation vs neoplastic plexopathy

clinical: neoplastic more painful


timing: neoplasm acute and faster, radiation delayed and slower


location: radiation involve supper plexus, malignancy involves lower plexus


EMG: myokymia in radiation, both have neurogenic changes


imaging will show infiltrating lesion/ass in malignancy, rads may be normal or some T2hyper

Innervation and cause of damage in following nerves: long thoracic, suprascapular, axillary and musculocutaneous nerves

Long thoracic (C5-7) = serratus anterior, due to brachial neuritis, surgery, trauma


Suprascapular: weak in supra and infraspinatus, due to repetitive stretch injury


Axillary: deltoid, trauma


Musculocutaneous: biceps, due to trauma

Median nerve: list branches and innervation

Motor: PT, FCR, FDS, FDP, FPL, PQ, LOAF


AIN: FDP1/2, FPL, PQ (test pronation with arm flexed)


Sensory: palmar branch


Median neuropathy


In antecubital fossa: rare, weak in all muscles


AIN: pure motor, weakness of FPL, FDP 2,3, PQ


At wrist: CTS

Ulnar nerve: list branches and innervation

Motor: FCU, FDP 3,4, LOAF of digit minimi, FDI, Adductor pol


Sensory: DUC, palmar cutaneous branch, terminal branches


Ulnar neuropathy


At elbow: very common, affects all ulnar, benediction sign-clawing of D4/5, froment’s sign-weak FDI/Ad Pol


At wrist: spares sensory of dorsal ulnar hand and medial palm. Spares FCU and FDP

Radial nerve

Triceps, BR, ECR, Supinator, ECU, EDS, EDM Abd pol, Ext pol, EIP


PIN: pure motor, involves everything distal to Supinator

Radial neuropathies

Axilla – crutches/compression- entire radial nerve affected


spiral groove/Saturday night palsy: spares triceps


PIN neuropathy: pure motor, spares triceps and ulnar wrist extension (wrist radially deviated) finger extensors, thumb extension impaired


Superficial radial sensory neuropathy/handcuff beuropathy: dorsum of the hand numb

CTS risk factors, clinical features, treatment and prognosis

RF: pregnancy, DM, hypothyroid, acromegaly, HNPP, RA, masses, amyloid, renal failure


Clinical features, nocturnal paresthesias, numbness, weakness, phalen, tinnel


Treat: wrist splint, surgery if progressive/severe symptoms

Radic vs nerves: muscle to differentiate bw: C6/median, c7/radial, C8/ulna

C6 vs median: non median C6 brachioradialis (radial)


C7 vs radial: brachioradialis (radial not C7)


C8 vs ulnar: non ulnar C8: FPL (median), EIP (radial)

Lumbosacral plexus: compare upper vs lower plexus weakness

Upper plexus: L2-L4, weak hip flexion, adduction, knee extension


lower plexus: L5-S3: weak hip abduction, extension, knee flexion, all ankle muscles

femoral nerve innervation

HF (iliacus), KE (quads:rectus femoris, vastus lateralis, intermedium and medialis)


Sensory: medial cut nerve of thigh