Emg

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most common source of error in EMGs

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cooler temperatures --> slow conduction and increase amplitudeage below 5 years and above 60heightstimulation errors

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temperature effect on EMG

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cooler temperature slow conduction 1.5-2.5 m/s per 1 degree celsius drop in temperature

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effect of age on EMG

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age 3-5 is when peripheral myelination reaches adult valuesafter age 60 --> 0.5-4 m/s per decadeSNAP amplitudes may drop by 50% by age 70

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effect of height on EMG

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taller individuals have slower CVsnerves taper in size with lengthdistal limbs are coolermost relevant for F-waves

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types of myelinated nerve fibers

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cutaneous afferents --> 6-12um --> 35-75m/smuscle afferents --> 12-21um --> 80-120m/smuscle efferents --> 6-12um --> 35-75m/sunmyelinated fibers --> 0.2-1.5um --> 1-2m/s

Front 6

which fibers are measured in NCS

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large myelinated fibers which account for 20% of nerve fiberssmall fiber neuropathies may have normal NCS

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SNAP

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sensory nerve action potentialonset latency --> represents the largest/fastest fibersamplitude --> sum of all fibers that depolarizeduration is about 1.5ms compared to 5-6ms for motor

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CMAP

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compound motor action potentialdistal latencyamplitude --> number of muscle fibers that depolarizeconduction velocityduration --> measures synchrony of depolarization

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antidromic response

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going towards the spinal cordF-wave

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F response

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antidromicstimulates anterior horn cellsrepresents 1-5% of all muscle fiberspure motor responsecan be only abnormal finding in GBS

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hoffman response

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it's a reflexafferents --> Ia muscle spindlesefferents --> alpha motorneurons and axonselicited from tibial nervehelpful for S1 radic, LS plexopathies, sciatic mononeuropathy

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pure axonal neuropathy findings

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reduced amplitude --> axonal lossconduction velocity not less than 75% of lower limit of normal (not less than 37.5 m/s)distal latency not more 130% increased

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pure demyelinating neuropathy findings

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conduction velocity < 75% of lower limit of normal (lower limit of normal 50 m/s)distal latency markedly prolongued > 130%conduction blocktemporal dispersion

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conduction block

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proximal CMAP amplitude is reduced by 20% or more compared to distal CMAP amplitudeand/or increase in duration > 20%implies acquired demyelinating process

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temporal dispersion

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decrease in amplitude > 20% and increased duration > 20%slower fibers lag behing faster fibersimplies acquired demyelinating processmore prominent with sensory fibers

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hereditary demyelinating neuropathies

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Charcot Marie Tooth 1 --> Hereditary Motor and Sensory Neuropathy 1Charcot Marie Tooth 3 --> Hereditary Motor and Sensory Neuropathy 3 --> Dejerinne-SottasRefsum disease --> Hereditary Motor and Sensory Neuropathy 4Hereditary Neuropathy with Liability to Pressure Palsies (HNPP)metachromatic leukodystrophyKrabbe'sadrenoleukodystrophyCockayne syndromeNiemann-Pick disease

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AIDPCIDP --> HIV, MGUS, anti-MAG, Waldenstrom macroglobulinemiamultifocal motor neuropathy with conduction block (GM1 antibody)diptheriatoxins

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AIDP first EMG sign

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delayed, absent or impersistent F waves --> proximal demyelination

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AIDP EMG findings

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delayed or absent F waveprolongued distal latency, conduction block, temporal despersion in 50% by two weeks, 85% by three weeks90% have motor involvement > sensorysural nerve sparing even with abnormal median, ulnar and radial SNAPs

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CIDP EMG findings

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prolongued DL, slow CV, conduction block, temporal dispersiondecreased amplitudesneedle EMG --> large MUAPs, reduced recruitment

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conduction velocity of SNAPs

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no neuromuscular junction so may be taken from a single pointmay use onset latency or peak latency

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conduction velocity of CMAPs

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need to account for neuromuscular junction --> difference between proximal and distal latencies

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positive waves

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spontaneous discharge of one muscle fiberregular frequencypositive deflectionabnormal acute/ongoing denervationdull pop sound

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fibrillations

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spontaneous discharge of one muscle fiberregular frequencyabnormal --> acute/ongoing denervationinitial positive deflection spikesound like rain on roof or metronome

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EPS Vs. fibs

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end plate spikes --> spike morphology, initial neg deflection, irregular, "frying", normal findingfibs --> spike morphology, initial positive deflection, regular, "rain", abnormal

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end plate noise

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small monophasic negative deflectionsoccur spontaneously at NMJminiature end-plate potentialsnormal findinghissing/seashell sound

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needle findings of denervation

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fibs and positive wavescan occur in neuropathic or myopathic processes

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occurence of fibs and positive waves

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neuropathiesinflammatory myopathiesbotulismmuscular dystrophies

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myotonic discharges

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single fiber repetitive discharges with smooth progression of frequency and amplitudeprovoked by needle insertion, tapping on muscle or gripingpathognomonic of myotonias"dive bomber" sound

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fasciculation

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spontaneous irregular repetitive discharge of single motor unitpathognomonic for anterior horn or proximal root diseasecan be benign or pathologicpathologic --> in the presence of postitive waves and fibs

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neuromyotonia

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high frequency iregular discharges grouped into irregular burstssingles, doublets and tripletscaused by hyper excitability of peripheral axons which results in discharges of motor units or fibersping sound

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myokimia

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irregular repetitive discharges of groups of motor unitslooks like different muscles flickering

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when are fasciculations pathologic

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only when there are positive waves and fibs present as well

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where is the lesion in fasciculations

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anterior horn cells or proximal root

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conditions associated with myokimia

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radiation-induced nerve injuryfacial myokimia --> GBS, MS, pontine tumors

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neuropathic MUAP

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reduced recruitment and very large amplitudes

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myopathic MUAP

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increased recruitment and very small amplitudes

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acute axonal MUAP

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duration --> normalphase --> normalamplitude --> normalrecruitment --> reduced

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chronic axonal MUAP

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duration --> prolongedphase --> polyphasicamplitude --> increasedrecruitment --> reduced

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demyelinating MUAP

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duration --> normalphase --> normalamplitude --> normalrecruitment --> normal

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demyelinating + conduction block MUAP

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duration --> normalphase --> normalamplitude --> normalrecruitment --> reduced

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acute myopathy MUAP

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duration --> shortphase --> polyphasicamplitude --> smallrecruitment --> early

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chronic myopathy MUAP

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duration --> prolongedphase --> polyphasicamplitude --> smallrecruitment --> reduced

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large myelinated fibers

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Aα --> diameter 12-21μ --> 80-120 m/sAβ --> diameter 6-12μ --> 35-75 m/smeasured in NCS

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small myelinated fibers

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Aδ --> diameter 1-5μ --> 5-30 m/sB --> diameter 3μ --> 3-15 m/snot measured in CNS

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fiber type --> hair follicle

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Aβ

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fiber type --> skin follicle

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Aβ

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fiber type --> muscle spindle

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Aα

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fiber type --> joint receptor

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Aβ

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fiber type --> pain and temperature

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Aδ, C

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fiber type --> preganglionic efferent

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B

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fiber type --> postganglionic efferent

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C

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fiber type --> afferent to DRG

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C

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fibers measured in NCS

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large myelinated fibers Aα and Aβ

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fibers not measure in NCS

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small myelinated and unmyelinated fibers Aδ, B and C

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chanels at the axon membrane

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voltage-gated sodium channels

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nodes of ranvier

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space between segments of Schwan cell axon ceveragethis is where depolarization occursvoltage-gated sodium channels are concentrated at nodes of ranvier

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most commonly studied upper extremity nerves

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medianradialulnar

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most commonly studied lower extremity nerves

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peronealsuraltibial

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units for motor NCS

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millivolts

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units for sensory NCS

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microvolts

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mixed nerves typically studied in NCS

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medianulnardistal tibial

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MNAPs

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mixed nerve action potentials

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features of mixed nerve actions potentials

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median, ulnar and distal tibialinclude stimulation of the largest/fastest myelinated fibers Aα (Ia)typically conduction velocities are faster and usually Ia fibers first to be affected by demyelination due to their size

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fibers that contribute to amplitude and area

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all large myelinated fibers

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fibers that contribute to distal latency and conduction velocity

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only the fastest fibersusually myelinated fibers are normally distributed between speeds of 35-65m/s, with most being around 50m/sdistal latency and CV is given mostly by the fastest fibers

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why is there no abnormal slowing in pure axonal neuropathies?

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normal limit 50-60 m/s reflects the fastest conducting fibers from a normal distribution of fibers between 35-65 m/s75% of the lower limit of 50 m/s is about 37.5 m/sat 75% of lower limit (37.5 m/s) therefore there are still myelinated axons contributing to the CV, while amplitude will be decreasedanything slower while also having decreased amplitude, means mixed axonal-demyelinating neuropathyin reality, pure axonal neuropathies affect all axons within the normal distribution without being selective, fastest, slowest and averageif therre is no axon, there is no myelin!

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pseudo conduction block Vs conduction block

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pseudo conduction block is axonal --> in hyperacute axonal injury (< 3 days), stimulating proximal to the lesion will show decreased amplitude when recorded distal to the lesionconduction block is demyelinating

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hyperacute axonal injuries such as nerve transection

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if stimulated and recorded distal to the lesion, NCS will be nornal as transected axon still functions until Wallerian degeneration ensuesif stimulated proximal to the lesion and recorded distally --> pseudo conduction block

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phase cancellation

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seen in SNAPs, normal phenomenonslower sensory fibers lag behind the fastestby the time the slower fibers reach the electrode after proximal stimulation, the fastest fibers are getting farther leaving behind a positive deflectionthe positive deflection of the moving-away fastest fibers, cancels out some of the negative deflections of the nearing-in slowest fibers

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late responses

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F responseH response

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nerves for F response upper extremities

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median and ulnar

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nerves for F response lower extremities

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peroneal and tibial

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pure motor late response

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F response

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F response measurements

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minimal latency --> the F response with shortest latency out of ten, represents fastest fibersmaximal latency --> the F response with longest latency out of ten, represents slowest fiberschronodispersion --> difference between minimal and maximal latenciesF wave persistence --> number of F responses obtained per 10 stimulations, usually ~ 80-100%, always above 50%

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what does F response represent

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1-5% of muscle fibers from a small population of motor neuronsevery stimulation fires a different population of motor neuronsCMAP and morphology will mostly be different between them

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minimal latency

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the F response with shortest latency out of ten, represents fastest fibers

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maximal latency

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the F response with longest latency out of ten, represents slowest fibers

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chronodispersion

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difference between minimal and maximal latenciesnormal is 4ms in UE and 6ms and LE

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F wave persistence

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number of F responses obtained per 10 stimulations, usually ~ 80-100%, always above 50%

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F response utility

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can only detect C8-T1 (abductor policis brevis and minimi) and L5-S1 radiculopathies (distal peroneal and tibial-innervted msucles)even for those roots, the utility is limited

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where is the H reflex ellicited?

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only at the tibial nerve in popliteal fossa (gastroc-soleus muscle)

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circuitry of H reflec

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afferent --> muscle spindle Ia (Aα) sensory fibersefferent --> α motor neurons

Front 84

which root is evaluated by the H reflex?

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S1H reflex is the electrical correlate of the ankle reflex