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NCV AND EMG
This document provides an overview of nerve conduction studies and electromyography. It discusses the anatomy and neurophysiology relevant to understanding these diagnostic tests. The key points covered include: 1) Nerve conduction studies and electromyography are used to diagnose disorders of the peripheral nervous system including motor and sensory neurons, nerve roots, plexuses, nerves, neuromuscular junctions and muscles. 2) The tests provide information about the fiber types involved, the underlying nerve pathophysiology, and help narrow the differential diagnosis. 3) The document reviews the fundamentals and principles of nerve conduction studies and electromyography including motor, sensory and mixed nerve conduction studies and the patterns that can indicate conditions like ax
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NCV AND EMG
- 1. NERVE CONDUCTION STUDIES, ELECTROMYOGRAPH YDR.SUBODH KUMARMAHTO PGIMER,DR.RML HOSPITAL, NEW DELHI
- 2. CONTENTS • Approachto NCS and EMG • Anatomy and Neurophysiology • Fundamentals of NCS – Basic Nerve conduction studies – Late Responses – Blink Reflex – Repititive Nerve Stimulation • Fundamentals of EMG – Basic Overview – Analysis of Spontaneous Activity – Analysis of Motor Unit Action Potentials (MUAP) • Clinical- ElectrophysiologicCorrelations
- 3. Approach • Serveas an extension of the clinical examination. • Directed neurologic examination essential before EDX studies to identify clinical abnormalities and establish a DD. • Individualized, based on DD & modified in real time as the study progresses & further information gained.
- 4. • Used todiagnose disorders of the peripheral nervous system – primary motor neurons (anterior horn cells), – sensory neurons (dorsal root ganglia), – nerve roots, – brachial and lumbosacral plexuses, – peripheral nerves, – neuromuscular junctions, and – muscles. • Provide diagnostic information when disorder arises in CNS (e.g., tremor/ upper motor neuron weakness).
- 5. Localization is the aimof EDx study The Primary motor neuron resides within the spinal cord, whereas the primary sensory neuron, the dorsal root ganglion, lies outside the spinal cord.The dorsal root ganglion is a bipolar cell. lts proximal process forms the sensory nerve root; the distal process becomes the peripheral sensory nerve.
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- 7. Nerve conduction studies oftenprovide further valuable information about the fiber types involved and the underlying nerve pathophysiology and narrow the differential diagnosis
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- 12. • The peripheralnervous system includes • the peripheral motor and sensory neurons; their • primary neurons, the anterior horn cells, and dorsal root ganglia; • the neuromuscular junctions; and • muscle. • The DRG, a bipolar cell located distal to the sensory root, is anatomically different from the anterior horn cell. • Consequently, lesions of the nerve roots result in abnormalities of MNCs but spare the SNCs, as the dorsal root ganglion and its peripheral nervee remain intact.
- 13. • The motorroot( from AHCs), leaves ventrally • Sensory root enters the dorsal side. • Distal to the DRG, the motor and sensory roots together- form spinal nerve. • Each spinal nerve divides- a dorsal and ventral ramus. • Each ramus contains both motor and sensory fibers. • The dorsal rami supply sensation to skin over back. • The ventral rami • continue as intercostal nerves in the thoracic region. • In the lower cervical region, the ventral rami fuse to form the brachial plexus. • In the mid lumbar through sacral segments, intermix to form the lumbosacral plexus.
- 15. Myotomal and peripheral nerveinnervation Dermatomes
- 16. individual peripheral nerve anatomy Myelinated fibers-small dark rings (myelin) with a central clearing (axon). The endoneurium is present between axons. Axons grouped into fascicles, surrounded by perineurium (arrow). Surrounding the entire nerve- epineurium (large arrow).
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- 19. Motor unit • Themotor unit- one axon, its anterior horn cell & all connected muscle fibers and NMJs. • A nerve fiber AP always results in depolarization of muscle fibers of motor unit creating an electrical potential known as the motor unit action potential (MUAP). • Analysis of motor unit action potentials- needle EMG examination.
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- 21. Important points to ponder • Routinemotor & sensory conduction velocity & latency measurements from the largest & fastest fibers. • Small myelinated (Adelta, B) & unmyelinated C -not recorded with standard NCSs- neuropathies that preferentially affect only small fibers may not reveal any abnormalities. • Largest & fastest fibers , muscle afferents, Alpha fibers (aka Ia fibers)-originate from muscle spindles & mediate afferent arc of muscle stretch reflex- not recorded in either MNCs & SNCs.
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- 23. • Process ofintracellular electrical potential being transmitted through extracellular fluid and tissue. • volume-conducted potentials • near-field • far-field potentials. • Near-field potentials can be recorded only close to their source, depend on distance between recording electrodes & electrical source (AP). CMAPs, SNAPs, and MUAPs, recorded during routine motor conduction, sensory conduction, and needle EMG studies- examples. Volume Conduction
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- 26. BASIC NERVE CONDUCTION STUDIES • Motorconduction studies • Sensory conduction studies • Mixed conduction studies • Basic patterns
- 27. Motor conduction studies • Performed first •Responses in range of mV (sensory &mixed- microV) • Less affected by technical factors • Gain set at 2-5mV • Recording elecrodes- belly tendon montage – G1 (active)- centre of muscle belly – G2 (reference)- over tendon • Stimulus over supplying nerve with cathode closest to electrode. – Characteristics- duration-200 microS, current 20-50mA. – Supramaximal stimulus essential (starting from baseline) – Gradually increased till max potential recorded. – Further 20% increase to ensure supramaximal stim. • Recorded potential- CMAP (biphasic)
- 28. CMAP Latency • Time fromstimulus to initial deflection from baseline • Represents- – Time from stimulus site to NMJ – Time delay across NMJ – Depolarisation across muscle Amplitude • From baseline to neg peak/ 1st neg to 1st pos peak • Reflects no of muscle fibres that depolarise • Decreased amplitude – Loss of axons – Conduction block – NMJ disorders – Myopathies Duration • From deflection from baseline to 1st baseline crossing • Measure of synchrony • Increased with slowing of some fibres but not others
- 29. Conduction velocity • DL represents: –the nerve conduction time from the distal stimulation site to the NMJ (A), – NMJ transmission time (B) – muscle depolarization time (C). • PL represents – distal nerve conduction time (A), – the NMJ time (B) – muscle depolarization time (C) – nerve conduction time between the proximal and distal stimulation sites (D). • DL subtracted from PL =nerve conduction time between the distal and proximal stim sites (D) • conduction velocity=(distance/time). • CV reflects only fastest fibers
- 30. Sensory conduction studies • Only nervefibres assessed (no NMJ, no muscle) • Response very small (1-50microV) • Gain set 10-20 microV • Recording eletrodes (G1 and G2) n line 3-4 cm apart • Stiumulus characteristcs – Duration 100/200 microS – Current- 5-30 mA to supramaximal stimulus(less threshold than motor) • Recorded potential- SNAP (biphasic/triphasic) • CV measured from 1 stim site
- 31. SNAP Latency- Onset &Peak • Onset – time from stim to initial neg deflect (biphasic), to the positive peak (triphasic). Represents time from stim site to electrodes for fastest conducting fibres • Peak- measured at the mid point of 1t neg peak. Easier to measure Amplitude • From baseline to neg peak. • Reflects sum of all individual sensory fibres that depolarise • Low values- def disorder of peripheral nv Duration Conduction velocity • From onset to 1st baseline crossing • Typically shorter than CMAP (1.5 ms vs 5-6 ms)
- 32. CMAP VS SNAP diff interms of size & duration. CMAP amplitude measured in mV, whereas SNAPs in microvolt range (different gains). CMAP negative peak duration 5 to 6 ms, whereas SNAP’s much shorter, typically 1 to 2 ms..
- 33. Orthodromic vs antidromic recording Top trace: Antidromicstudy, stimulating wrist, recording index finger. Bottom trace: Orthodromic study, stimulating index finger, recording wrist
- 34. Advantages & Disadvantages • Advantages ofantidromic over orthodromic – Amplitude of SNAP higher – Helpful in pathological conditions. – Less subject to noise/artifacts. • Disadvantages – SNAP f/b volume conducted CMAP – Difficult to differentiate if sensory latency is increased.
- 35. Lesions Proximal to theDorsal Root Ganglion Result in Normal Sensory Nerve Action Potentials
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- 37. Explanation • SNAPs& CMAPs both compound potentials, represent summation of individual fiber APs. • Some fibers that conduct faster & some more slowly . – With distal stimulation, fast and slow fiber potentials arrive recording site at approximately same time. – proximal stimulation, slower fibers lag behind faster fibers. • For sensory fibers, neg phase of the slower fibers overlaps with pos trailing phase of fastest fibers. cancel each other, resulting in decrease in area & amplitude • Less for motor potentials d/t their large amplitude & smaller range of normal CVs
- 38. Temporal dispersion and phase cancellation Proximal sensoryfiber potentials cancel out each other Phase cancellation not significant for CMAPs because of their large amplitude.
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- 40. • Largest &fastest fbres, Ia, spindle afferents recorded only in mixed studies. • Entire nerve stimulated & recorded • CVs faster. • Ia fibres have highest myelin content, earliest affected in demyelinating neuropathies (entrapment). • Settings- – Gain set at 10-20microV – Recording electrodes (G1 G2) placed in line at distance 3- 4 cms – Mixed Nerve Action Potential (MNAP)- summation of all sensory and MFAPs- biphasic/triphasic.
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- 42. BASIC PATTERNS 1. Axonal 2. Demyelination 3.Myopathy 4. NMJ disorders
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- 44. Patterns B: Axonal loss.amplitudes decrease;CV is normal/slightly slowed, but not < 75% LLN & DL is normal or slightly prolonged, but not >130%ULN. morphology doesn’tchange between proxim and distal sites A: Normal study. Note the normal DL <4.4 ms, amplitude >4 mV and CV >49 m/s. C: Demyelination- unifom, slowing often associated with inherited conditions (e.g.,CMT polyneuropathy). CV markedly slowed < 75% LLN) & DL markedly prolonged (>130% ULN). No change in config between proxim and distal stimulation sites. D: Demyelination with CB/temporal dispersion. Marked slowing of CV and DL with change in morphology between distal and proxim stimulation sites associated with acquired causes of demyelination, may be seen in GBS
- 45. CV slowing in Axonal loss fastest-65 m/s slowest- 35 m/s
- 46. Demyelination • Essentially,any motor, sensory, or mixed nerve conduction velocity that is slower than 35 m/s in the arms or 30 m/s in the legs signifies unequivocal demyelination. Dilemma- which is what? • Might appear that reduced amplitudes always marker of axonal loss rather than demyelination. Not true, depends on: • first, whether sensory or motor studies are performed, and • second, whether or not conduction block is present. • Sensory amplitudes low in demyelinating lesions. Reduced sensory amplitudes from normal temporal dispersion and phase cancellation, exaggerated by demyelinative slowing
- 47. Conduction block • Reduced amplitudesin demyelination seen when CB is present, as in acquired demyelination . • If CB is present in demyelinating lesion,CMAP amplitude depends on stimulation site & location of CB – CB b/w normal distal stim site & recording electrodes, both distal and proximal CMAP amplitudes low and may simulate an axonal loss lesion – CB b/w distal and proxim stim sites,CMAP amplitude normal distally, below block, but decreased at proxim stim site, above block. – Proximal & distal stim sites distal to block,CMAP amplitudes- normal both distally and proximally
- 48. Conduction Block In acquireddemyelinating lesions, demyelination often patchy, multifocal process. When nerve stimulated proximal to the conduction block, the compound muscle action potential (CMAP) drops in ampl-itude and area and becomes dispersed (
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- 50. Million dollar question- CBor Temporal dispersion? use criteria of mare than 50% drop in area between proximal and distal stimulation sites to define electrophysiologic CB. remember that both CB and abnormal temporal dispersion and phase cancellation signify acquired demyelination. • A marked drop in proximal CMAP area usually means conduction block. • In the figure, there is no conduction block between distal and proxim stim sites. Drop in amplitude entirely due to abnonnal temporal dispersion from demyelinating lesion. • To differentiate conduction block from abnormal temporal dispersion requires drop in area >50%.
- 51. Two patients with wrist drop-who has the better prognosis? • Patient 1- conduction block- demyelination- better prognosis • Patient 2- significant axonal loss with some CB across the spiral groove- prognosis guarded
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- 53. Myopathy • Sensoryconduction studies- always normal unless a/w superimposed neuropathic condition. • Motor conduction studies- most myopathies primarily affect proximal muscles. – CMAP amplitudes and distal latencies- generally normal ( routine MNCS record distal muscles). – Rare myopathic disorders affect distal muscles, and in such situations CMAP amplitudes- low. – Even in these situations, however, DL and CVs- normal.
- 54. NMJ Disorders • Sensory conductionstudies- always normal • Motor conduction studies- – postsynaptic- normal – Presynaptic-CMAPs low at rest, CVs and DL normal. •For diagnosis- RNS/ Exercise testing.
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- 57. F Response circuitry • nervestimulated distally - depolarization occurs both orthodromically & antidromically. – Direct muscle response (M)- orthodromic. – F response(F)- derived by antidromic travel to AHC-- backfiring of some AHCs---orthodromic travel back down nerve past stimulation site to muscle • Actually a smallCMAP, representing 1-5% of muscle fibres • Circuitry, both afferent & efferent- pure motor • No synapse- not a true reflex. • Sensory neuropathy- F respose normal • Settings- gain increased to 200 microV and the sweep to either 5 or 10 ms. • Measurements- minimal / maximal latency, persistence, chronodispersion.
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- 59. Contd.. • With proximalstimulation, proximal CMAP latencies increase as expected, but F response latencies decrease, d/t F response first traveling antidromically to spinal cord. • Each F response varies slightly in latency, config & amplitude- diff population of AHCs being activated with each stimulation. • shortest latency-largest and fastest motor fibers. • Best obtained with distal stim
- 60. Contd.. • Fwave persistence- – measure of no of F waves obtained per number of stimulations. – Normal-80% to 100% & always above 50%. • F wave chronodispersion- – diff betwn fastest & slowest F response. – Normal-up to 4 ms in the UL & up to 6 ms in LL. • Minimal F wave latency- most reliable measurement • F responses- absent in sleeping/sedated patients- absent responses not necessarily sign of pathology.
- 61. Do F waves assessonly proximal segment? • Prolonged responses – Any nerve with prolonged DL on routine NCS – Generalized CV slowing in polyneuropathy – Prolonged in legs than arms – Taller patients • Factors affecting F wave response – DL – CV – Height NO
- 62. So, Can’t we diagnose proximal lesionswith F? F ESTIMATE F estimate = (2D/CV) x 10 + 1 ms + DL X -time from stim site to cord; distance between stim site and cord (D) divided byCV of the nerve Y-turnaround time at AHC= 1 ms Z-time from stim site to the muscle= DL Theoretical F estimate = 2X +Y + Z. X can be calculated by measuring the .Thus, the F estimate = (2D/CV) x 10 + 1 ms + DL
- 63. • Normally, Festimate > minimal F wave latency (CV is more in prox segments) • Therefore, if the measured minimal F response is prolonged compared to the F estimate • delay in proximal nerve segments out of proportion to what can be expected for DL, CV & height.
- 64. USEFULNESS OF F RESPONSE • Teststhe entire nerve circuit. • Greatest usefulness in early acquired demyelinating polyradiculopathies- combo of normal routine NCS + prolonged F response suggesting proximal lesion where demyelination starts. • NOTE- F response 1-5% of CMAP, so unobtainable with severely reduced CMAP( axonal loss)
- 65. For Radiculopathy & Plexopathy? • Limitedd/t following reasons – F responses can check only nerve/nerve root that innervating muscle being recorded. • In the upper extremity, distal muscles (i.eAPB, ADM)- innervated by C8/T1 nerve roots, rarely affected by radiculopathy, compared with commonly affected C5, C6, C7- • usefulness only in assessing possibleC8-Tl radiculopathies & L5-S1 radiculopathies – In radiculopathy predominantly affecting sensory nerve root fibers (initial symptoms of pain and radiating paresthesias),F response-normal.
- 66. Bottomine of F response •If distal nerve conductions are normal, prolonged F response may occur in – proximal neuropathy, – plexopathy, or – radiculopathy, and • the finding cannot be used to differentiate among those possibilities.
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- 68. • True reflex-sensory afferent, synapse & motor efferent segment. • H reflex in adults can routinely be elicited only by stimulating tibial nerve in the popliteal fossa, recording the gastro-soleus muscle. • The circuitry of the H reflex involves the – Ia muscle spindles as sensory afferents and the – a motor neurons and their axons as efferents. • Low sub maximal stimulus with a long duration selectively activates the Ia fibers.
- 70. SUBMAXIM AXIMAL STIM BEST ELICITS H REFLEX •at low stimulation intensities, H reflex present without direct motor (M) response. • With increasing stimulation, H wave grows & M response appears. • At higher stimulation, M potential continues to grow & H reflex diminishes, d/t collision betwn the H reflex & antidromic motor potentials.
- 71. MEASUREMENTS & APPLICATIONS • Hreflex with shortest latency measured & compared with set of normal controls for height • Comparison with C/L side more useful in assessing U/L lesion; difference >1.5 ms-considered significant. • Max amplitude H response compared with maximal amplitude M potential to calculate H/M ratio • USEFULNESS – electrical correlate of S1 ankle reflex. If ankle reflex present clinically, H reflex should always be present. – Any lesion that might decrease ankle reflex also might prolong the H reflex (polyneuropathy, proximal tibial and sciatic neuropathy, lumbosacral plexopathy & lesions of the 51 nerve root). – H/M ratio-crude assessment of AHC excitability- increased in UMN lesions.
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- 75. NMJ • Electrical-chemical-electrical barrier. • Presynaptic terminal-Ach in vesicles ka quanta (each ha 1000 molecules) • 3 separate stores- – Immediately available store (1000 quanta) – Mobilization store (10000 quanta) – Reserve store (>100000 quanta) • Process of transmission • AP depolarizes presynaptic junction Ca influx via volt gated channels quanta released Ach binds receptors on post synaptic membrane opens Na channels, local depolarization-EPP above threshold causes MFAP • Normally, EPP always above threshold by a margin (safety factor)
- 76. Effect of RNS in normal subjects •Slow RNS (2-3 Hz) Quanta progressively depleted from primary store EPP amplitude falls still above threshold d/t safety factor MFAP with each stimulation after few seconds, mobilisation store repletes quanta,increasing EPP with MFAP • Rapid RNS quanta depleted takes 100 ms to actively pump out Ca RNS leads to accumulation of Ca wich counterbalances quanta depletion along with mobilization store EPP increase MFAP
- 77. EPP threshold>15 mV Rapid (50 HZ)RNS presynaptic disorder- progressive increment of EPP amplitude to above threshold and subsequent gen of MFAP
- 78. Exercise Testing- equivalent of Rapid RNS •Post exercise facilitation (brief period of exercise,10 s)- effect identical to RNS – Normal –consistent generation MFAP-CMAP – Postsynaptic- causes EPP to increase • EPP above threshold at baseline- no change • EPP below threshold- causes repair. – Presynaptic- facilitates low EPPs- usually EPP below threshold at baseline- MFAP is generated when nitially there was none. • Post exercise exhaustion- (mechanism not understood)- after 1 min of max voluntary exercise rises initially f/b fall over several min. • Normal- EPP falls but never below threshold. • NMJ disorders- Prolonged exercise- greater decline- MFAP not generated
- 79. 3HzRNS in MG. •A: Decrement of CMAP amplitude at rest. • B: Postexercise facilitation, Decrement of CMAP immediately following 10 seconds of maximal voluntary exercise has repaired toward normal. • C-E: Postexercise exhaustion. Decrements of CMAP 1, 2, and 3 minutes after 1 minute of maximal voluntary exercise. Decrement becomes progressively more marked over the baseline decrement. • F: Postexercise facilitation after a decrement. Immediately following another 10 seconds of maximal voluntary exercise, the decrement, which has worsened as a result of postexercise exhaustion, repairs toward normal.
- 80. RNS in MG •the large decrement between the first and fourth potentials. • After the 4th potential,the decrement not as marked- forms "U shape." • Decrement begins to improve when the mobilization store resupplies immediately available store. • Requires I to 2 secs • highly characteristic of a true NMJ disorder.
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- 82. ELECTROMYOGRAPHY Analysis of SpontaneousActivity Analysis of Motor Unit Action Potential
- 83. Clinical implications of spontaneous activity • Distribution ofabnormal activity- neuroanatomic localization.(isolated radiculopathy, denervation potentials restricted to muscles in same myotome). • Type of spontaneous activity- specific diagnostic information. (Myotonic discharges- few myopathies, hyperkalemic periodic paralysis) • Degree or amount of spontaneous activity determine severity. • Information about time course.(radiculopathy, several weeks pass before fibrillation potentials seen)
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- 86. • A: Miniatureendplate potential (monophasic negative). • B: Muscle fiber action potential, brief spike morphology.Triggered by needle-induced depolarization of terminal nerve twig (initial negative, diphasic). • C: Muscle fiber action potential, brief spike morphology (initial positive, triphasic). • D: Muscle fiber action potential, positive wave morphology (initial positive, slow negative). • E: Multiple different muscle fiber action potentials linked together. • F: Motor unit action potential. Note the longer duration and higher amplitude compared with MFAP shown above.
- 87. Insertional activity • With eachneedle movement, normal insertional activity- brief &usually lasts </= 300 ms • Increased insertional activityseen in both neuropathic & myopathic disorders.
- 88. Waveform morphology and site of depolrization •A:Traveling depolarizing wave create a biphasic potential if begins under recording needle electrode (initial negative peak) & then moves away from electrode (positive peak).This is known as an endplate spike. • B: If begins at a distance from the needle. there is initial positive deflection as it moves toward needle, f/b negative phase as it moves beneath needle, and then final positive deflection as it travels away.This is known as a fibrillation potential. • Endplate spikes are differentiated from fibrillation potentials by the absence of an initial positive deflection because the depolarization begins at the endplate.
- 89. Spontaneous activity- normal • All spontaneousactivity is abnormal exception-that occurs at NMJ- END PLATE NOISE, END PLATE SPIKES • End plate noise (seashell sound) • End plate spikes(cracking, sputtering)
- 90. Abnormal spontaneous activity Fibrillation potentials • MFAPmorphology-Brief spike initial pos deflection, 1-5 ms duration, low amplitude (10-100 microV). • Regular, rate 0.5-10 Hz, sound like "rain on the roof.“ • Typically seen in neuropathic disorders Positive sharp waves • signify active denervation. • brief initial positivity f/b long negative phase. • sound “dull pop”, amplitude variable (10-100 microV), regular firing, with a rate 0.5-10 Hz, up to 30 Hz. • Graded from 0 to 4+
- 91. Contd.. Complex repetitive discharges •multiple spikes (each spike representing different single muscle fiber) • perfectly repetitive nature, machine like sound • In chronic neuropathic/myopathic disorders; arise in any setting- denervated muscle fibers lie adjacent to other denervated muscle fibers. Myotonic discharges • Myotonic discharges-seen in myotonic dystrophy, myotonia congenita, paramyotonia congenita. • "rewing engine" sound on EMG, due to waxing-waning. • a single brief run may occur in any denervating disorder
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- 93. Typical MUAP morphology Fasciculations (corn poppingsound), doublets Myokymic discharges (radiation induced nerve damage)
- 94. Cramps and neuromyotonic discharges NEUROMYOTONIC DISCHARGES high-frequency(150-250 Hz), decrementing, repetitive discharges of single motor Unit, "pinging" sound CRAMPS high-frequency discharges of motor axons, with the electromyogram characteristically showing MUAPs with a normal morphology firing repetitively & sometimes irregularly at high frequencies.
- 95. Rest tremor vs myokymia Rest tremor Myokymicdischarges (marching sound)
- 96. Analysis of motor unit action potentials (MUAP) •Attributes of MUAP- – Morphology • Duration • No of phases • Amplitude – Stablity – Firing characteristics • Patterns- – normal – Neuropathic – myopathc
- 97. Morphology (based on mean ofat least 20 different MUAPs in a muscle) • Duration- – Best reflects no of muscle fibres within a motor unit – 5-15 ms – From initial deflection from baseline to return to baseline – Duration correlates with pitch • Long duration sound dull and thuddy, short duration crisp and static like • Polyphasia, serrations & satellite potentials – Polyphasia –measure of synchrony • Normally MUAPS-2-4 phases • Increased polyphasia in 5-10% in any muscle-N • Polyphasic MUAPs- high frequency clicking • Non specific – Serrations- changes in direction that do not cross baseline. Same implication as polyphasia – Satellite potentials- in early reinnervation.
- 98. • Amplitude varieswidely. Most MUAPs have an amplitude >100 microV & < 2 mV. measured from peak to peak – Increased amplitude with (1) proximity of the needle to the motor unit (2) increased no of muscle fibers in motor unit (3) increased diameter of muscle fibers (4) more synchronized firing of muscle fibers. • Major spike- largest positive to negative component of MUAP
- 99. • Stability- measureof effective NMJ transmission. Unstable MUAPs seen in NMJ disorders/immature NMJs (eary reinnervation). • FIRING FREQUENCY – Activation- ability to increase firing rate. (central process) – Recruitment- increase in no of firing motor units. Affected in neuropathies. – Interference pattern • Normal ratio of firing frequency to no of motor units firing 5:1.
- 100. Normal firing pattern Semirhythmic pattern Relationship offorce to firing frequency. Maximal firing rate- 30Hz
- 101. Interference patterns • A: Normal •B: Neuropathic. • C: Myopathic. • In normal subjects, so many motor unit action potentials (MUAPs) fire during maximal contraction that differentiating individual motor unit potentials is difficult. • In neuropathic recruitment, a reduced number of MUAPs fire at a high frequency, resulting in an incomplete interference pattern (often called the picket fence pattern). • In myopathic recruitment, although the number of MUAPs is normal, the interference pattern consists of short-duration, small amplitude MUAPs.
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- 103. Poor activation or poor recruitment?• In the trace, the same unit (identical morphology) firing rapidly (30 Hz) • Ratio-30:1- poor recruitment- neuropathic pattern Patient asked to contract maximally • In the trace, the same unit (identical morphology) firing at 5 Hz • Ratio-5:1- normal recruitment- but poor activation- central disorder (uncooperative/stroke, MS)
- 105. • Normal MUAPshave two to four phases. • In chronic neuropathic lesions (after reinnervation), no of muscle fibers/motor unit increases- long- duration/high-amplitude/ polyphasic MUAPs. • In myopathies/NMJ disorders with block, the no of Junctional muscle fibers in motor unit decreases-short- duration/ small-amplitude/ polyphosic MUAPs.
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- 107. Important points • Time course- –Hyperacute- <3 days – Acute-more than several days but less than 2 weeks – Subacute- less than several months – Chronic- months- years • Wallerian degeneration starts in 3-5d . • Denervation potentials in 2-6 weeks • Reinnervation is complete in months-years
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